Biological Psychology 11E By JAMES Kalat - Test Bank

Biological Psychology 11E By JAMES Kalat – Test Bank

 

Instant Download – Complete Test Bank With Answers

 

 

Sample Questions Are Posted Below

 

Chapter 5: Development and Plasticity of the Brain

 

TRUE/FALSE

 

1. The human central nervous system begins to form when the embryo is about 10 weeks old.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1                               TOP:   5.1 Development of the Brain

 

2. Once the brain is fully developed, the anatomy of the brain is unchanging.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1                               TOP:   5.1 Development of the Brain

 

3. The fluid-filled cavity within the neural tube becomes the central canal of the spinal cord and the four ventricles of the brain.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1                               TOP:   5.1 Development of the Brain

 

4. Proliferation is the production of new cells.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1                               TOP:   5.1 Development of the Brain

MSC:  www

 

5. Axons are usually formed before the dendrites.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1                               TOP:   5.1 Development of the Brain

 

6. After cells have differentiated as neurons or glia, they migrate.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1                               TOP:   5.1 Development of the Brain

 

7. An early and fast stage of neuronal development is myelination.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 2                               TOP:   5.1 Development of the Brain

 

8. Some neurons provide the myelination for other neurons.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 2                               TOP:   5.1 Development of the Brain

 

 

 

 

9. Myelination of the brain and spinal cord is complete by the time of birth.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 2                               TOP:   5.1 Development of the Brain

 

10. Synaptogenesis is a process that begins before birth and continues throughout life.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 2                               TOP:   5.1 Development of the Brain

MSC:  www

 

11. Recent evidence suggests that adult vertebrate brains generate new neurons.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 2                               TOP:   5.1 Development of the Brain

MSC:  www

 

12. The number of neurons in the brain is continually increasing throughout life.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 2                               TOP:   5.1 Development of the Brain

 

13. Mammals and amphibians are similar in that they can both easily generate new axons.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 2                               TOP:   5.1 Development of the Brain

 

14. The brain requires millions of chemicals to correctly guide the growth of axons to their target locations.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 2                               TOP:   5.1 Development of the Brain

MSC:  www

 

15. Apoptosis is distinct from necrosis, which is death caused by an injury or a toxic substance.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

16. Nerve growth factor is a chemical that promotes the survival and activity of neurons.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

MSC:  www

 

17. The developing infant brain is highly resistant to damage.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ: 3                               TOP:   5.1 Development of the Brain

 

 

18. Physical exercise is important for increased dendrite growth and branching.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Fine-Tuning by Experience       OBJ: 4             TOP:              5.1 Development of the Brain

 

19. Exercise may account for some of the neural benefits that come from rearing rats in an enriched environment.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Fine-Tuning by Experience       OBJ: 4             TOP:              5.1 Development of the Brain

MSC:  www

 

20. A rat in a more stimulating environment develops a thicker cortex, more dendritic branching, and improved learning.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Fine-Tuning by Experience       OBJ: 4             TOP:              5.1 Development of the Brain

 

21. The most common cause of brain damage in children is closed head injury.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

22. In strokes caused by ischemia or hemorrhage, neurons die from overstimulation.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 1 TOP:              5.2 Plasticity After Brain Damage

 

23. The damaging effects of a stroke can be limited if treated within a short period of time.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 1 TOP:              5.2 Plasticity After Brain Damage

 

24. Diaschisis refers to the decreased activity of surviving neurons after damage to other neurons.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage               MSC:  www

 

25. One effective method to overcome diaschisis after brain damage is to administer stimulant drugs.

 

ANS:  T                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

26. An axon in the peripheral nervous system is more likely to recover after being cut than if it is crushed.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

27. Paralysis caused by spinal cord injury is usually only temporary in humans.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

MSC:  www

 

28. Denervation supersensitivity results from the disuse of incoming axons.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

29. Recent evidence suggests that phantom limb pain is caused by sensations coming from the stump of the amputated limb.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage MSC:     www

 

30. Deafferentation of the left arm results in the inability to move it.

 

ANS:  F                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

 

 

MULTIPLE CHOICE

 

1. The ability of the brain to change its anatomy over time, within limits, is known as:

a.	plasticity.
b.	regression.
c.	connectivity.
d.	long term potentiation.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Introduction     OBJ: 1 TOP:     5.1 Development of the Brain

 

2. Early in development, the nervous system begins as a:

a.	tube surrounding a fluid-filled cavity.
b.	spherical structure in the center of the embryo.
c.	diffuse system of cells scattered throughout the body.
d.	single layer of cells covering the heart and other internal organs.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

3. The human central nervous system:

a.	begins to form during the fetal stage.
b.	is unlike all other vertebrate central nervous systems in its developmental process.
c.	begins to form when the embryo is about two weeks old.
d.	begins to form when the embryo is about two months old.

 

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

4. As the neural tube sinks under the surface of the skin, the forward end enlarges and differentiates into the:

a.	spine, midbrain, and forebrain.
b.	hindbrain, midbrain, and forebrain.
c.	hindbrain, midbrain.
d.	midbrain, forebrain.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

5. When do the ventricles and the central canal of the spinal cord form?

a.	shortly after birth in humans
b.	just as the forebrain starts its rapid phase of growth
c.	early in embryonic development
d.	during the third trimester

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

6. The fluid-filled cavity of the developing neural tube becomes the:

a.	forebrain.
b.	midbrain.
c.	spinal cord.
d.	ventricular system.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

7. What is the production of new neurons called?

a.	differentiation
b.	migration
c.	myelination
d.	proliferation

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

8. Stem cells are important for which of the following developmental processes?

a.	migration
b.	proliferation
c.	myelination
d.	synaptogenesis

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain                     MSC:  www

 

 

 

 

 

9. Proliferation is the:

a.	production of new cells.
b.	movement of primitive neurons and glia.
c.	formation of dendrites and an axon.
d.	insulation process that occurs on some axons.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain                     MSC:  www

 

10. Proliferation occurs:

a.	at the top of the spinal column.
b.	around the vesicles.
c.	around the ventricles.
d.	at the expanding edge of the brain.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

11. After cells have differentiated as neurons or glia, they:

a.	differentiate.
b.	proliferate.
c.	myelinate.
d.	migrate.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

12. Chemicals known as ____ and ____ guide neuron migration.

a.	immunoglobulins; sodium
b.	glia; neurothrophins
c.	immunoglobulins; chemokines
d.	chemokines; neurothrophins

 

 

ANS:  C                    PTS:   1                    DIF:    conceptual      REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

13. What term describes the movement of primitive neurons and glia within the developing nervous system?

a.	Differentiation
b.	Migration
c.	Myelination
d.	Proliferation

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

14. Which of the following would most likely interfere with migration of neurons during development?

a.	altering the chemical paths
b.	damaging dendrites
c.	loss of myelin
d.	increased differentiation

 

 

ANS:  A                    PTS:   1                    DIF:    conceptual      REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

15. Migration is the:

a.	production of new cells.
b.	movement of primitive neurons and glia.
c.	gradual formation of dendrites and an axon.
d.	insulation process that occurs on some axons.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

16. Immunoglobulins and chemokines play an important role in neural:

a.	migration.
b.	proliferation.
c.	synaptogenesis.
d.	apoptosis.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

17. Which of the following best characterizes how axons arrive at the correct target cells?

a.	They follow electrical gradients.
b.	They follow chemical gradients from the target cell.
c.	Axons send out chemicals to the target cells.
d.	Target cells send out branches for the axons to follow.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Pathfinding by Axons

OBJ: 2 TOP:              5.1 Development of the Brain

 

18. Migration requires:

a.	a precise chemical environment.
b.	cells which are myelinated.
c.	mature neurons.
d.	neurons with fully developed dendrites.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

19. Differentiation is the:

a.	production of new cells.
b.	movement of primitive neurons and glia.
c.	formation of dendrites and an axon.
d.	insulation process that occurs on some axons.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

20. What is the process called when a primitive neuron begins to develop dendrites and an axon?

a.	Differentiation
b.	Migration
c.	Myelination
d.	Proliferation

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

21. The formation of a neuron’s distinctive shape occurs during the ____ stage of neurogenesis.

a.	proliferation
b.	migration
c.	differentiation
d.	myelination

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

22. Whether or not a transplanted immature neuron adopts the properties of neurons in the new location or retains at least some properties of neurons from where it was taken from depends largely on how much the transplanted neuron has:

a.	myelinated.
b.	proliferated.
c.	migrated.
d.	differentiated.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

23. After the migrating neuron reaches its destination, ____ begin to form.

a.	dendrites
b.	axons
c.	nuclei
d.	ganglions

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain                     MSC:  www

 

24. Myelination is a process common to:

a.	all vertebrate axons.
b.	all vertebrate dendrites.
c.	some vertebrate axons.
d.	some invertebrate axons.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

25. For some axons, glial cells produce an insulating sheath that makes rapid transmission possible. What is this process called?

a.	Differentiation
b.	Migration
c.	Myelination
d.	Proliferation

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

 

26. In humans, myelination first occurs in the:

a.	spinal cord.
b.	hindbrain.
c.	midbrain.
d.	forebrain.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain                     MSC:  www

 

27. Myelination in the human brain:

a.	is complete upon birth.
b.	is complete around the second birthday.
c.	is complete sometime shortly after adolescence.
d.	continues well into the adult years.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

28. The stages of neurogenesis that occur for the longest duration are:

a.	myelination and synaptogenesis.
b.	proliferation and myelination.
c.	migration and proliferation.
d.	differentiation and migration.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

29. The final stage of neurodevelopment is called:

a.	synaptogenesis.
b.	differentiation.
c.	migration.
d.	fusion.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

30. The formation of new synapses is called:

a.	synaptogenesis.
b.	differentiation.
c.	migration.
d.	fusion.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1         TOP:              5.1 Development of the Brain

 

31. New neurons are known to develop in all of the following cases EXCEPT:

a.	olfactory receptors.
b.	the human corpus callosum.
c.	the brain area responsible for birdsong.
d.	hippocampus of mammals.

 

 

 

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1                               TOP:   5.1 Development of the Brain

KEY: NEW

 

32. As a rule, all vertebrate neurons develop during an embryological stage. Among the few types of neurons that can develop in adulthood are:

a.	ganglion cells in the retina.
b.	olfactory receptors.
c.	motor nerves in the spinal cord.
d.	long-axoned neurons of the primary motor cortex.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1                               TOP:   5.1 Development of the Brain

 

33. Brain cells that are neither neurons nor glia, but which are capable of dividing and then differentiating into neurons or glia, are called:

a.	parallel fibers.
b.	intrinsic cells.
c.	stem cells.
d.	glomeruli.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Maturation of the Vertebrate Brain        OBJ: 1                               TOP:   5.1 Development of the Brain

 

34. What happened when Weiss grafted an extra leg onto a salamander adjacent to one of the hindlegs?

a.	The new leg gradually took over for the old.
b.	The new leg withered and died.
c.	Nerves from the old leg attached to the new in a random fashion.
d.	Branches of axons from the old leg attached to corresponding muscles in the new.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Pathfinding by Axons

OBJ: 2                      TOP:   5.1 Development of the Brain

 

35. What process occurs when axons attempt to form connections to a grafted limb in a salamander?

a.	Axons connect randomly, but only muscles “tuned” to the right message respond.
b.	Axons connect randomly and muscles learn to coordinate through experience.
c.	Axons find their way to corresponding muscles in the new leg.
d.	A lack of nerve growth fiber leads to the degeneration of the new leg.

 

 

ANS:  C                    PTS:   1                    DIF:    conceptual      REF:   Pathfinding by Axons

OBJ: 2                      TOP:   5.1 Development of the Brain

 

36. If you cut the optic nerve of a newt, what happens?

a.	The fibers grow back and attach to random targets, so they see a scrambled picture.
b.	The fibers grow back and attach to their original targets, resulting in normal vision.
c.	The newt remains blind, since neurons do not regenerate.
d.	The fibers attach to multiple targets, resulting in blurry vision.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Pathfinding by Axons

OBJ: 2                      TOP:   5.1 Development of the Brain

 

37. Chemicals in the amphibian tectum guide the growth of axons from the retina to their correct location in the tectum by:

a.	having dozens of different growth factors.
b.	using an electrical gradient.
c.	using a chemical gradient.
d.	glial cell transportation.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Pathfinding by Axons

OBJ: 2                      TOP:   5.1 Development of the Brain

 

38. Roger Sperry cut a newt’s optic nerve and rotated the eye. Axons from what used to be the dorsal part of the retina (now located on the ventral side) grew back to the target areas:

a.	that ordinarily get input from the dorsal retina.
b.	that ordinarily get input from the ventral retina.
c.	that ordinarily get input from the center of the retina.
d.	equally and diffusely.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Pathfinding by Axons

OBJ: 2                      TOP:   5.1 Development of the Brain

 

39. When Sperry cut a newt’s optic nerve and rotated the eye by 180 degrees, each axon:

a.	degenerated.
b.	regenerated to a random location.
c.	regenerated to the area where it had originally been.
d.	regenerated, but to the area appropriate to its new location.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Pathfinding by Axons

OBJ: 2                      TOP:   5.1 Development of the Brain           KEY: NEW    MSC:   www

 

40. What visual capabilities did Sperry’s newt have after Sperry cut the optic nerve and rotated the eye?

a.	It regained normal vision.
b.	It saw the world upside down and backwards.
c.	It required experience to relearn how to see.
d.	It remained blind.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Pathfinding by Axons

OBJ: 2                      TOP:   5.1 Development of the Brain

 

41. Which of the following best describes the process by which developing axons find their general target areas?

a.	completely random growth
b.	shape attraction
c.	electrical attraction
d.	chemical attraction

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Pathfinding by Axons

OBJ: 2                      TOP:   5.1 Development of the Brain

 

42. Axons sort themselves over the surface of the target area:

a.	by following a gradient of chemicals.
b.	through apoptosis.
c.	through necrosis.
d.	based on their size.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Pathfinding by Axons

OBJ: 2                      TOP:   5.1 Development of the Brain           MSC:  www

 

43. Which of the following are selective as axons form synapses with target cells?

a.	axons, but not target cells
b.	target cells, but not axons
c.	both axons and target cells
d.	neither axons nor target cells

 

 

ANS:  C                    PTS:   1                    DIF:    conceptual      REF:   Pathfinding by Axons

OBJ: 2                      TOP:   5.1 Development of the Brain

 

44. Competition of neurons for postsynaptic sites results in survival of only the most successful axons. This general principle is called:

a.	natural selection.
b.	evolution.
c.	apoptosis.
d.	neural Darwinism.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Pathfinding by Axons

OBJ: 2                      TOP:   5.1 Development of the Brain           MSC:  www

 

45. The concept that neurons refine their many connections based on which ones are most successful is known as:

a.	natural selection.
b.	evolution.
c.	survival of the fittest.
d.	neural Darwinism.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Pathfinding by Axons

OBJ: 2                      TOP:   5.1 Development of the Brain

 

46. What is meant by neural Darwinism?

a.	The brains of higher primates are the ones that are most similar to those of humans.
b.	Most individual differences in the brain are due to genetic mutations.
c.	Successful neurons develop while less successful neurons weaken or die.
d.	Successful neurons reproduce while less successful neurons do not.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Pathfinding by Axons

OBJ: 2                      TOP:   5.1 Development of the Brain

 

47. ____ steer new axonal branches and synapses in the right direction.

a.	Chemokines
b.	Immunoglobulin
c.	Glia
d.	Neurotrophins

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

MSC:  www

 

48. Why is it that all neurons in a healthy adult brain have made appropriate connections?

a.	Chemical messages from our muscles tell our brain how many neurons to form and that number perfectly matches the connections required.
b.	If an axon does not make the appropriate connections by a certain age, it dies.
c.	We are born with all connections formed.
d.	Connections form rapidly, but we learn to use whatever connections have formed.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

49. Why is it that every axon in an adult mammal has a target cell (muscle cell or other neuron) with which it makes synaptic contact?

a.	Each target cell causes the growth of a neuron and its axon.
b.	After formation, axons release a chemical that causes a target cell to form.
c.	Axons that fail to find a target cell die.
d.	An axon will make contact with any kind of cell and adjust its function as necessary.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

50. What is signaled by nerve growth factor (NGF)?

a.	That a target cell has “accepted” an axon
b.	Which target cell a growing axon should connect with
c.	That axons should elongate as the body grows bigger
d.	The need for new neurons to form in brain areas that are lacking in neurons

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

51. Nerve growth factor (NGF):

a.	promotes the survival and growth of the axon.
b.	is a fuel metabolized by neurons.
c.	promotes programmed cell death.
d.	is a hormone first released at puberty.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

52. Necrosis:

a.	is a programmed mechanism of cell death.
b.	is cell death caused by an injury or a toxic substance.
c.	promotes the survival and growth of dendrites.
d.	promotes the activity of neurons.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

53. Apoptosis:

a.	is a programmed mechanism of cell death.
b.	promotes the survival and growth of the axon.
c.	promotes the survival and growth of dendrites.
d.	promotes the activity of neurons.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

54. If a sympathetic nervous system axon does not receive enough nerve growth factor, the neuron will:

a.	kill itself.
b.	grow a shorter axon.
c.	compensate by growing more dendrites.
d.	decrease its velocity of action potentials.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

55. What is apoptosis?

a.	the growth of an axon in response to NGF
b.	the leakage of transmitters from vesicles
c.	a program of “suicide” by a neuron
d.	dendritic branching in the sympathetic nervous system

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

56. Some neurons die during development because:

a.	they are surrounded by glia.
b.	they do not receive enough GABA.
c.	they receive too much NGF.
d.	they fail to receive enough NGF.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

57. The function of neurotrophins is to:

a.	inhibit proliferation.
b.	promote survival of axons.
c.	be used as fuel.
d.	signal that an axon has been “rejected.”

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

MSC:  www

 

58. Which of the following is NOT a function of neurotrophins?

a.	Direct axonal growth during development.
b.	Increase axonal branching in mature neurons.
c.	Increase regrowth of axons after brain damage.
d.	Induce apoptosis of neurons.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

59. Developing neurons need ____ for survival.

a.	neurotrophins only
b.	neurotrophins and synaptic input
c.	synaptic input only
d.	apoptosis

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

 

60. An axon that does not receive enough neurotrophins from a target cell will:

a.	branch out and form other synapses on other cells.
b.	manufacture its own neurotrophins.
c.	degenerate and die.
d.	fail to reabsorb transmitters that have already been released.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

61. In development, neurotrophins ____.  During adulthood, they ___.

a.	preserve neurons; produce apoptosis
b.	produce apoptosis; increase neuronal branching
c.	facilitate differentiation; facilitate migration
d.	preserve neurons; increase neuronal branching

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

62. At later stages of the neuron’s development, neurotrophins:

a.	increase the branching of axons.
b.	cause the neuron’s death.
c.	become converted into myelin.
d.	connect the axon to axons of adjoining cells.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

63. Which statement most accurately describes embryonic development of the nervous system in humans?

a.	The majority of cells remain as primitive neurons until birth.
b.	All synapses that are formed are permanent.
c.	Neurons form before birth; synapses form after birth.
d.	Far more neurons are produced than will ultimately survive.

 

 

ANS:  D                    PTS:   1                    DIF:    conceptual      REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

64. In response to nervous system injury, neurotrophins:

a.	cause the neuron’s death.
b.	reduce inflammation due to this injury.
c.	increase regrowth of damaged axons.
d.	promote apoptosis.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

65. Massive cell death in the brain during prenatal development is:

a.	an indication of a genetic abnormality.
b.	an indication of restricted blood flow to the fetus.
c.	usually due to an autoimmune disorder.
d.	normal.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

66. The most likely explanation for the excess proliferation of neurons in early development is that it:

a.	compensates for connection errors.
b.	uses up excess stored fuel.
c.	increases learning capacity when it is most needed.
d.	prevents apoptosis.

 

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

67. For survival, developing neurons need:

a.	neurotrophins only.
b.	neurotrophins and synaptic input.
c.	synaptic input only.
d.	apoptosis.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

68. Compared to an adult, a fetus has:

a.	more neurons.
b.	approximately the same number of neurons.
c.	about half the number of neurons.
d.	about one-tenth the number of neurons.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

69. After maturity, the apoptotic mechanisms become:

a.	hyperactive.
b.	extinct.
c.	dormant.
d.	very complex.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Determinants of Neuronal Survival       OBJ: 2                               TOP:   5.1 Development of the Brain

 

70. An iodine deficiency in the diet can lead to an inadequate production of thyroid hormones. What is the result if this occurs in an infant or developing fetus?

a.	Down’s syndrome
b.	mental retardation
c.	Tourette’s syndrome
d.	accelerated body growth

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ:           3                    TOP:   5.1 Development of the Brain

 

 

71. What modern day practice helps prevent an inadequate production of thyroid hormones?

a.	fluoride in drinking water
b.	processed sugar
c.	iodized salt
d.	artificial sweeteners

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ:           3                    TOP:   5.1 Development of the Brain

 

72. In infants, anesthetic drugs can increase:

a.	proliferation.
b.	migration.
c.	myelination.
d.	apoptosis.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ:           3                    TOP:   5.1 Development of the Brain

MSC:  www

 

73. Children of mothers who drink heavily during pregnancy are born with:

a.	fetal alcohol syndrome
b.	Turner’s syndrome
c.	Klinefelter’s syndrome
d.	PKU

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ:           3                    TOP:   5.1 Development of the Brain

 

74. The mechanism of fetal alcohol syndrome probably relates to:

a.	overexcited neurons.
b.	apoptosis.
c.	decreases apoptosis.
d.	necrosis.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ:           3                    TOP:   5.1 Development of the Brain

 

75. What condition would be suspected if a young child shows decreased alertness, hyperactivity, mental retardation, motor problems, a heart defect, and abnormal facial features?

a.	fetal alcohol syndrome
b.	Turner’s syndrome
c.	Klinefelter’s syndrome
d.	PKU

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ:           3                    TOP:   5.1 Development of the Brain

 

76. The most likely reason that children with fetal alcohol syndrome have brain abnormalities is because alcohol:

a.	overexcites neurons.
b.	stimulates nerve growth factor.
c.	decreases apoptosis.
d.	decreases release of neurotrophins.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ:           3                    TOP:   5.1 Development of the Brain

 

77. What brain abnormalities are found in children with fetal alcohol syndrome?

a.	short axons with few branches
b.	short dendrites with few branches
c.	lack of dopamine receptors
d.	smaller than normal ventricles

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ:           3                    TOP:   5.1 Development of the Brain

MSC:  www

 

78. Alcohol suppresses the release of ____, the brain’s main excitatory transmitter.

a.	5-HT
b.	DA
c.	GABA
d.	glutamate

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ:           3                    TOP:   5.1 Development of the Brain

 

79. How much alcohol, if any, can a pregnant woman drink without worrying about the negative effects on her child?

a.	The equivalent of two cocktails a day
b.	The equivalent of one beer a day
c.	Anything less than what causes her to act drunk
d.	Unknown, and therefore abstention is recommended

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ:           3                    TOP:   5.1 Development of the Brain

 

80. Alcohol can damage the developing brain by:

a.	tearing the cell membrane.
b.	increasing synaptic inhibition and therefore apoptosis.
c.	overstimulating neurons.
d.	interfering with protein production.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ:           3                    TOP:   5.1 Development of the Brain

 

81. Children of mothers who use cocaine during pregnancy:

a.	have a slightly higher birth weight.
b.	are likely to develop Turner’s syndrome.
c.	have a slightly lower IQ score.
d.	are born with severe abnormalities resembling cerebral palsy.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   131

OBJ:   3                    TOP:   5.1 Development of the Brain – The Vulnerable Developing Brain

MSC:  www

 

82. Children of mothers who smoke cigarettes during pregnancy are at an increased risk of:

a.	intellectual deficits.
b.	Korsakoff’s syndrome.
c.	Rett syndrome.
d.	Parkinson’s disease.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   131

OBJ:   3                    TOP:   5.1 Development of the Brain – The Vulnerable Developing Brain

 

83. On average, exposure to nicotine during pregnancy increases risk of ____ deficits.

a.	emotional
b.	attention
c.	learning
d.	memory

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ:           3                    TOP:   5.1 Development of the Brain

KEY:  NEW

 

84. Which of the following, if any, would be more damaging to an adult brain than to the brain of an infant or fetus?

a.	Exposure to alcohol
b.	Infections like German measles
c.	Iodine deficiency in the diet
d.	All of these are more damaging to an infant brain.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   The Vulnerable Developing Brain         OBJ:           3                    TOP:   5.1 Development of the Brain

 

86. Keeping animals in a varied environment with stimulation increases the:

a.	branching of dendrites.
b.	speed of action potentials.
c.	density of Nodes of Ranvier along the axon.
d.	thickness of axons.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Fine-Tuning by Experience       OBJ:    4           TOP:              5.1 Development of the Brain

 

 

 

 

 

 

87. The areas of the cortex used by expert video game players are most likely to ____ than the same cortical areas of those who don’t play video games.

a.	be thicker
b.	have smaller, but a greater number of neurons
c.	have faster action potentials
d.	be more resistant to transcortical stimulation

 

 

ANS:  A                    PTS:   1                    DIF:    conceptual      REF:   Fine-Tuning by Experience       OBJ:    4           TOP:              5.1 Development of the Brain

 

88. Which of the following aspects of brain and neural functioning can be most clearly altered by experience?

a.	velocity of action potentials
b.	structure of dendrites and axons
c.	chemical constituents of the ventricles
d.	number of laminae in the cerebral cortex

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Fine-Tuning by Experience       OBJ:    4           TOP:              5.1 Development of the Brain

 

89. What is different about rats raised in an enriched environment in comparison to rats raised in an impoverished environment?

a.	a more pleasant personality
b.	improved learning performance
c.	better parenting skills
d.	nothing

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Fine-Tuning by Experience       OBJ:    4           TOP:              5.1 Development of the Brain

 

90. Research in people over age 60 who were randomly assigned to experience six months of aerobic exercise showed:

a.	that they developed more axons.
b.	that they developed less tumors.
c.	that they developed greater thickness of the cortex.
d.	that they developed less thickness of the cortex.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Fine-Tuning by Experience       OBJ:    4           TOP:              5.1 Development of the Brain

 

91. Which of the following factors seems to be particularly important for branching of neurons during brain development?

a.	Physical activity
b.	Playing logic games
c.	Having good teachers
d.	Having a sterile environment

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Fine-Tuning by Experience       OBJ:    4           TOP:              5.1 Development of the Brain

MSC:  www

 

 

92. Brain studies of blind people suggest that they have greater attention to touch and auditory stimulation because:

a.	cortical areas for touch and audition are thicker.
b.	their visual cortex is used for touch and verbal tasks.
c.	they have greater neural branching.
d.	they have greater neurotrophin release.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Fine-Tuning by Experience       OBJ:    4           TOP:              5.1 Development of the Brain

 

93. An MEG study of professional musicians listening to pure tones showed that:

a.	professional musicians had brain responses that were twice as strong as non-musicians.
b.	professional musicians had slightly less brain responses as non-musicians.
c.	professional musicians had drastically less brain responses as non-musicians.
d.	professional musicians had brain responses five times as strong as non-musicians.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Fine-Tuning by Experience       OBJ:    4           TOP:              5.1 Development of the Brain

 

94. Musicians who use the left hand to finger the violin strings have some alterations in one brain area, which is the:

a.	left hemisphere prefrontal cortex.
b.	right hemisphere prefrontal cortex.
c.	left hemisphere postcentral gyrus.
d.	right hemisphere postcentral gyrus.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Fine-Tuning by Experience       OBJ:    4           TOP:              5.1 Development of the Brain

 

95. Focal hand dystonia, sometimes called “musician’s cramp”, is caused by:

a.	extreme overlap of cortical representation of the fingers.
b.	deterioration of muscles in the hand.
c.	demyelination of neurons in the fingers.
d.	buildup of excess GABA in the temporal cortex.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Fine-Tuning by Experience       OBJ:    4           TOP:              5.1 Development of the Brain

 

96. Closed head injury is:

a.	the most common cause of brain damage in young adults.
b.	usually fatal.
c.	the most common cause of Korsakoff’s syndrome.
d.	related to Alzheimer’s disease.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery           TOP:              5.2 Plasticity After Brain Damage

 

97. The most common cause of brain damage in young people is:

a.	infection.
b.	gunshot wounds.
c.	stroke.
d.	closed head injury.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery           TOP:              5.2 Plasticity After Brain Damage

 

98. Closed head injury results in damage partially because of:

a.	increased production of myelin.
b.	excessive deficit of neurotrophins.
c.	rotational forces that push the brain against the inside of the skull.
d.	infection.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery           TOP:              5.2 Plasticity After Brain Damage

 

99. A sharp blow to the head resulting from an assault or trauma that does not actually puncture the brain is called a:

a.	stroke.
b.	cerebrovascular accident.
c.	hemorrhage.
d.	closed head injury.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery           TOP:              5.2 Plasticity After Brain Damage

 

100. Which of the following is the most common cause of a stroke?

a.	Lack of glucose
b.	Ischemia from an obstruction of an artery
c.	Hemorrhage of an artery
d.	Blow to the head

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

MSC:  www

 

101. A stroke caused by an artery rupturing is also known as:

a.	ischemia.
b.	hemorrhage.
c.	closed head injury.
d.	penumbra.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

102. Which of the following is not a cerebrovascular accident?

a.	Ischemia
b.	Hemorrhage
c.	Stroke
d.	Penumbra

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

 

 

 

103. A stroke which is caused when an artery ruptures is also known as:

a.	ischemia.
b.	hemorrhage.
c.	closed head injury.
d.	penumbra.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

104. Ischemia is to ____ as hemorrhage is to ____.

a.	older individuals; younger individuals
b.	proximal; distal
c.	obstruction; rupture
d.	barely noticeable; lethal

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

MSC:  www

 

105. What does edema mean?

a.	Lack of glucose
b.	Ischemia from an obstruction of an artery
c.	Hemorrhage of an artery
d.	Swelling due to accumulation of fluid

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

106. After a stroke, cells in the penumbra:

a.	are the first to die.
b.	help to remove dead or dying cells in the area of damage.
c.	quickly become more active, compensating for the area of damage.
d.	may die days or weeks after a stroke.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

107. After ischemia, neurons deprived of blood:

a.	transform from neurons into glia.
b.	lose much of their oxygen and glucose supplies.
c.	break down the blood-brain barrier.
d.	increase the velocity of their action potentials.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

KEY: NEW

 

108. ____ cells proliferate after a stroke.

a.	Penumbra
b.	Microglia
c.	Ischemia
d.	Cancer

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

KEY: NEW

 

110. Ischemia and hemorrhage kill neurons by:

a.	understimulating them.
b.	overstimulating them.
c.	overactivating the sodium-potassium pump.
d.	depleting the glutamate supply available to neurons.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

111. A stroke kills neurons in two waves, first by ____ and second by ____.

a.	overstimulation; understimulation
b.	Understimulation; overstimulation
c.	collateral sprouting; denervation supersensitivity
d.	denervation supersensitivity; collateral sprouting

 

 

ANS:  A                    PTS:   1                    DIF:    140                REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

112. Damage due to stroke caused by ischemia can be minimized by administering a drug that:

a.	breaks up blood clots.
b.	overstimulates neurons in and around the damaged area.
c.	increases the release of glutamate.
d.	slows down the sodium-potassium pump.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

113. Although the following methods may or may not actually work, which one would theoretically be of potential benefit to stroke victims?

a.	increasing activity at glutamate receptors
b.	opening sodium channels
c.	closing potassium channels
d.	blocking glutamate receptors

 

 

ANS:  D                    PTS:   1                    DIF:    conceptual      REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

114. Tissue plasminogen activator (tPA):

a.	is recommended for hemorrhage.
b.	overstimulates glutamate receptors.
c.	should be administered a few days after stroke.
d.	is helpful in cases of ischemia.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

 

 

115. Which of the following would be the best treatment for helping someone who is suffering from a stroke caused by a blood clot?

a.	decrease activity of the sodium-potassium pump
b.	warm the brain
c.	administer tPA
d.	enhance glutamate release

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

116. In research aimed at minimizing damage due to stroke, attempts to prevent overstimulation of cells have produced:

a.	very promising results.
b.	disappointing results.
c.	a complex interaction between age of patient and season of the year.
d.	positive results in humans, but not so for animals.

 

 

ANS:  B                    PTS:   1                    DIF:    conceptual      REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

117. Researchers have tried using drugs that block apoptosis. Results have been:

a.	favorable in animals and human trials.
b.	favorable in animal trials but too costly to try with humans.
c.	favorable in animal trials but difficult or impractical to apply to humans.
d.	unfavorable in all research trials.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

118. One approach in minimizing stroke damage in laboratory animals is the use of:

a.	calcium
b.	serotonin
c.	cannabinoids
d.	opioids

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 2 TOP:              5.2 Plasticity After Brain Damage

 

119. To date, the most effective laboratory method minimizing the damage resulting from stroke in nonhuman animals has been to:

a.	use drugs which trap free radicals.
b.	use drugs which effect cannabinoids.
c.	use neurotrophins which block apoptosis.
d.	cool the brain.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 1 TOP:              5.2 Plasticity After Brain Damage

 

120. In hemorrhage, cells in the penumbra:

a.	lose much of their oxygen.
b.	lose much of their glucose.
c.	are flooded with excess oxygen.
d.	act quickly to strengthen the blood-brain barrier.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 1 TOP:              5.2 Plasticity After Brain Damage

 

121. Research on laboratory animals indicates that cannabinoids are most effective if taken:

a.	as soon as the stroke occurs.
b.	within 20 minutes of the stroke.
c.	steadily for one month.
d.	shortly before the stroke.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Brain Damage and Short-Term Recovery                                 OBJ: 1 TOP:              5.2 Plasticity After Brain Damage    KEY: NEW

 

122. Diaschisis refers to the:

a.	increase in activity of neurons surrounding a damaged area.
b.	decreased activity of surviving neurons after other neurons are damaged.
c.	increased activity in the cerebral cortex after damage to any part of the brain.
d.	increased activity in the hypothalamus after damage to any part of the brain.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

123. A lesion in the hypothalamus can lead to decreased activity in the cerebral cortex, even though the cerebral cortex is undamaged. The decreased activity in the cortex because of the loss of incoming neurons is called:

a.	diaschisis.
b.	deafferentation.
c.	cytotoxicity.
d.	hyperpolarization.

 

 

ANS:  A                    PTS:   1                    DIF:    conceptual      REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

124. To promote recovery, stroke victims should be given:

a.	stimulant drugs immediately after the stroke.
b.	any drug that decreases dopamine.
c.	stimulant drugs a few days after the stroke.
d.	tranquilizers a few days after the stroke.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

125. Following a stroke, amphetamine could help by:

a.	inducing apoptosis.
b.	blocking activity in overstimulated areas of the brain.
c.	blocking glutamate release.
d.	increasing activity in understimulated areas of the brain.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

126. Which of the following treatments would be most likely to help a patient starting several days after a stroke?

a.	Injecting a drug to block dopamine
b.	Administering tranquilizers
c.	Extensive bed rest
d.	Giving stimulant drugs combined with physical therapy

 

 

ANS:  D                    PTS:   1                    DIF:    conceptual      REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

MSC:  www

 

127. Which axons will regenerate to a significant degree if cut or crushed?

a.	Those in invertebrates but not in vertebrates
b.	Only those which are unmyelinated
c.	Those in the central nervous system but not in the peripheral nervous system
d.	Those in the peripheral nervous system but not in the central nervous system

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

128. What is one impediment to regeneration of axons in the mammalian central nervous system?

a.	Inhibitory chemicals secreted by the damaged portion of the axon
b.	Bacterial infections caused by the decaying tissue
c.	Large amounts of scar tissue
d.	Inhibitory messages sent from the cell nucleus when an axon is damaged

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

129. A damaged axon:

a.	will never grow back.
b.	can grow back under certain circumstances.
c.	will grow back if its dendrites do also.
d.	will grow back only if it is myelinated.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

130. After a cut through the spinal cord, axons grow back enough to restore functioning in certain ____ but not in ____.

a.	adults; infants
b.	infants; adults
c.	fish; mammals
d.	mammals; primates

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

 

 

 

 

131. One limiting factor in the ability of damaged axons to regenerate in the brain and spinal cord is that:

a.	they don’t have any myelin to guide them.
b.	they regenerate only one to two millimeters.
c.	growing dendrites compete with growing axons.
d.	there are no muscles in the brain and spinal cord to guide the growth.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

132. Scar tissue and myelin are similar in that they both:

a.	secrete chemicals to restore axons.
b.	are produced after brain damage.
c.	are formed in normal development of the nervous system.
d.	secrete chemicals that inhibit axon growth.

 

 

ANS:  D                    PTS:   1                    DIF:    conceptual      REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

133. What is one impediment to regeneration of axons in the mammalian central nervous system?

a.	Inhibitory chemicals secreted by the damaged portion of the axon
b.	Bacterial infections caused by the decaying tissue
c.	Glia release chemicals that inhibit axon growth
d.	Inhibitory messages sent from the cell nucleus when an axon is damaged

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

134. One reason why axons regenerate better in the peripheral nervous system of mammals than in the central nervous system is that the peripheral nervous system:

a.	has fewer myelinated axons.
b.	has glial cells that destroy scar tissue.
c.	maintains a temperature closer to that at which embryonic cells form.
d.	produces a chemical that promotes axon growth.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

135. Central nervous system axons regenerate much better in fish than in mammals because fish:

a.	nerves do not have to travel so far to reach their target.
b.	myelin does not secrete proteins that inhibit axon growth.
c.	nerves have so much more myelin than do mammal nerves.
d.	myelin secretes a protein that accelerates regeneration.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

136. Central nervous system axons regenerate much better in fish than in mammals because:

a.	fish nerves do not have to travel so far to reach their target.
b.	fewer fish nerves are covered with myelin.
c.	fish do not produce as much scar tissue.
d.	fish generally have a lower body temperature.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

137. After central nervous system damage, myelin:

a.	degenerates and dies.
b.	secretes proteins that inhibit axon regrowth.
c.	secretes proteins that enhance some regrowth of axons.
d.	becomes thicker in surviving axons.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

138. If some of the axons innervating a given cell are destroyed or if they become inactive, what compensatory process takes place in the remaining presynaptic cells?

a.	activation of previously silent synapses
b.	removal of toxins
c.	denervation supersensitivity
d.	collateral sprouting

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

139. What is the term for the new branches that may form in uninjured axons after damage to surrounding axons?

a.	collateral sprouts
b.	bifurcations
c.	denervation supersensitivity
d.	diaschisis

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

MSC: www

 

140. After damaging input to the hippocampus, collateral sprouting is associated with improvements in:

a.	memory.
b.	taste.
c.	vision.
d.	hearing.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

141. After damage to a set of axons, neurotrophins induce nearby:

a.	injured axons to form new branches.
b.	injured dendrites to form new branches.
c.	uninjured axons to form new branches.
d.	uninjured dendrites to form new branches.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

142. If a tree branch is cut, the surrounding branches may grow enough to fill in the empty space left by the missing branch. When this same type of event occurs in the nervous system following brain damage, it is called:

a.	hemiplegia.
b.	denervation supersensitivity.
c.	collateral sprouting.
d.	tree branching.

 

 

ANS:  C                    PTS:   1                    DIF:    conceptual      REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

143. After damage to the connections to the left hippocampus from the left entorhinal cortex, sprouts develop from the:

a.	left occipital cortex.
b.	right entorhinal cortex.
c.	left hippocampus.
d.	right hippocampus.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

144. Heightened sensitivity to a neurotransmitter after the destruction of an incoming axon is known as:

a.	axon supersensitivity
b.	disuse supersensitivity
c.	enervation supersensitivity
d.	denervation supersensitivity

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

145. ____ helps compensate for decreased axon input.

a.	Axon supersensitivity
b.	Disuse supersensitivity
c.	Enervation supersensitivity
d.	Denervation supersensitivity

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

MSC:  www              KEY: NEW

 

146. Damage to some of the axons that innervate a given structure may give rise to:

a.	collateral sprouting, but not denervation supersensitivity.
b.	denervation supersensitivity, but not collateral sprouting.
c.	both collateral sprouting and denervation supersensitivity.
d.	neither collateral sprouting nor denervation supersensitivity.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

 

 

 

147. If most of the axons that transmit dopamine to some brain area die or become inactive, the remaining dopamine synapses become:

a.	less responsive.
b.	less easily stimulated.
c.	more resistant.
d.	more responsive.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage               KEY: NEW

 

148. After learning strengthens one set of synapses, other synapses:

a.	weaken.
b.	die.
c.	get stronger.
d.	become aroused.

 

 

ANS:  A                    PTS:   1                    DIF:    conceptual      REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage               KEY: NEW

 

149. In some cases, ____ enables people to maintain nearly normal behavior even after losing most of the axons in some pathway.

a.	receptor supersensitivity
b.	disuse supersensitivity
c.	extra supersensitivity
d.	response supersensitivity

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage               KEY: NEW

 

150. If a brain area loses a set of incoming axons, we can expect some combination of ____ by the remaining axons and collateral sprouting by other axons that ordinarily attach to some other target.

a.	disuse supersensitivity
b.	decreased response
c.	denervation supersensitivity
d.	response supersensitivity

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage               KEY: NEW

 

151. Certain axons innervating a given neuron are damaged. What compensatory change is likely to take place in that postsynaptic cell?

a.	collateral sprouting
b.	removal of toxins
c.	denervation supersensitivity
d.	decrease in glucose utilization

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

152. ____ occurs as a surviving axon grows a new branch to replace the synapses left vacant by a damaged axon.

a.	Collateral sprouting
b.	Degeneration supersensitivity
c.	Denervation supersensitivity
d.	Axon sprouting

 

 

ANS:  A                    PTS:   1                    DIF:    conceptual      REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage               KEY: NEW

 

153. If supersensitivity takes place, what can one expect to find regarding the number of receptors?

a.	An increased number in the presynaptic cell
b.	A decreased number in the presynaptic cell
c.	An increased number in the postsynaptic cell
d.	A decreased number in the postsynaptic cell

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

154. Denervation supersensitivity refers to an increase in:

a.	production and release of neurotransmitters.
b.	growth of axon branches.
c.	responses to neurotransmitters.
d.	polarization of the membrane at rest.

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

155. What is one reason for gradual behavioral recovery from brain damage?

a.	Uninjured areas of the brain develop new functions to take over the ones that were lost.
b.	Glia cells are transformed into neurons.
c.	Additional myelin forms on the axons that were not destroyed.
d.	Postsynaptic cells deprived of input become supersensitive.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

156. Suppose a finger is amputated. The part of the cerebral cortex that used to respond to that finger will:

a.	degenerate and die.
b.	remain alive but forever inactive.
c.	be active at times when the individual would have used that finger.
d.	become responsive to other fingers or part of the palm.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

 

 

 

 

157. A section of the somatosensory cortex ordinarily responds to the third finger of the left hand. If that finger is amputated, to what will the cells in this part of the cortex respond?

a.	Nothing
b.	The second and fourth fingers and part of the palm
c.	The third finger of the right hand
d.	The entire left hand and the entire right hand

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

158. Investigators recorded activity from the cerebral cortex of monkeys that had an entire limb deafferented twelve years earlier. Much to their surprise, what did they find?

a.	The organization of this area of the cortex had not been changed at all by the operation.
b.	This whole cortical area had become responsive to the face.
c.	This whole cortical area had become response to the opposite limb.
d.	This whole cortical area had developed motor instead of sensory functions.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

159. A cortical cell originally responded to stimulation of the middle finger. After amputation of that finger it begins responding to the second and fourth fingers. What most likely accounts for this?

a.	Synaptic reorganization
b.	Growth of completely new axons
c.	Altered pattern of blood vessels in the brain
d.	A psychotic reaction

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

160. A continuing sensation of an amputated body part is called:

a.	phantom limb
b.	ghost limb
c.	Neuralgia
d.	tingling limb

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

MSC:  www

 

161. After loss of sensory input from a limb, the axons representing that limb degenerate and:

a.	cause immediate cell death.
b.	leave vacant synaptic sites at several levels of the CNS.
c.	destroy any leftover synapses.
d.	cause no change in the associated neurons.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

 

 

162. The area of the cortex that receives input from the face is adjacent to the area of the cortex that receives input from the foot. After amputation of the foot, it is possible that a phantom limb sensation will be felt whenever the:

a.	other foot is touched.
b.	face is touched.
c.	face is anesthetized.
d.	axons from the foot regrow.

 

 

ANS:  B                    PTS:   1                    DIF:    conceptual      REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

163. Modern methods have demonstrated that phantom limbs develop only if the relevant portion of the ____ reorganizes and becomes responsive to alternative inputs.

a.	somatosensory cortex
b.	torso
c.	axon
d.	glia

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

KEY: NEW

 

164. Because spinal injury damages many axons, ____ develop increased sensitivity to the remaining ones.

a.	glia
b.	collateral sprouts
c.	postsynaptic neurons
d.	phantom limbs

 

 

ANS:  C                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage               KEY: NEW

 

165. Even _____ input produces enhanced responses.

a.	mild
b.	negative
c.	strong
d.	positive

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

KEY: NEW

 

166. Sensations from phantom limbs:

a.	come from the stump of the amputated limb.
b.	are a result of brain reorganization.
c.	do not have a neural basis.
d.	can be diminished if more of the limb is removed surgically.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

MSC:  www

 

167. One way to relieve the pain associated with a phantom limb is to:

a.	remove more of the amputated limb.
b.	have the amputee learn to use an artificial limb.
c.	stimulate that part of the cortex.
d.	help them understand that there is no neural basis for these sensations.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

168. If a person suffered injury to the right motor cortex that resulted in paralysis of the left arm and later showed some evidence of recovery of function, which of the following would be a likely explanation?

a.	Using the right arm more strengthened the left arm.
b.	The left motor cortex strengthened its control over the left arm.
c.	New neurons grew in place of the damaged ones.
d.	The left arm was deafferented.

 

 

ANS:  B                    PTS:   1                    DIF:    conceptual      REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

169. A monkey with one deafferented limb:

a.	cannot control the muscles of that limb.
b.	moves that limb whenever it uses its contralateral limb.
c.	uses it spontaneously, even though the animal has lost sensation to that body part.
d.	does not use it, even though it can still control the muscles.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

170. A deafferented limb:

a.	has lost its sensory input.
b.	has lost its motor control.
c.	is an amputated limb.
d.	is one which an organism uses spontaneously.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

171. After deafferenting a monkey’s forelimb, it generally fails to use it because:

a.	the muscles are too weak.
b.	moving it is painful.
c.	they have no motor control in the limb.
d.	walking on three limbs is easier than moving the impaired limb.

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

172. After damage to the visual cortex, a rat no longer approaches the white card it has been trained to approach. What is the evidence that the rat has not completely forgotten the task?

a.	It can relearn the task faster than it can learn to approach a black card.
b.	After a delay, it spontaneously regains the memory and approaches a white card.
c.	After several unreinforced sessions, it begins responding correctly.
d.	Its heart rate increases when looking at a white card but not when looking at a black card.

 

 

ANS:  A                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

173. If findings from rat studies generalize to humans, then which of the following best describes how brain damage affects memory for a learned skill?

a.	It destroys the memory forever.
b.	The memory is not affected.
c.	The memory may be present, but difficult to locate.
d.	The old memory is lost, but new ones are easier to acquire

 

 

ANS:  C                    PTS:   1                    DIF:    conceptual      REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

174. In dealing with brain-damaged patients, the usual goal is to:

a.	get the patients to rely on other people for the skills that they have lost.
b.	get the patients to make as much use as possible of the impaired systems.
c.	promote physical changes in the brain, such as collateral sprouting.
d.	encourage complete inactivity to enable the brain to engage in restorative processes.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

175. Who is most likely to assess the abilities of someone who has recently had brain damage?

a.	Neurosurgeon
b.	Physical therapist
c.	Occupational therapist
d.	Neuropsychologist

 

 

ANS:  D                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

176. In general, what can we say about recovery for brain-damaged patients in the future?

a.	There is very little hope of recovery.
b.	Researchers are optimistic, but they need to evaluate many possible therapies.
c.	Drug therapies have clear advantages over all other approaches.
d.	Brain grafts are the only real answer.

 

 

ANS:  B                    PTS:   1                    DIF:    factual            REF:   Later Mechanisms of Recovery             OBJ: 2         TOP:              5.2 Plasticity After Brain Damage

 

SHORT ANSWER

 

1. Define proliferation during neural development.

 

ANS:

This is the production of new cells. Early in development, the cells lining the ventricles of the brain divide. Some cells remain where they are, continuing to divide. Others become primitive neurons and glia that begin migrating to other locations.

 

PTS:   1                    DIF:    factual           REF:   Maturation of the Vertebrate Brain

OBJ:   1                    TOP:   5.1 Development of the Brain

 

 

2. Define differentiation during neural development.

 

ANS:

A primitive (simple) neuron forms its axon and dendrites, becoming a true neuron.

 

PTS:   1                    DIF:    factual           REF:   Maturation of the Vertebrate Brain

OBJ:   1                    TOP:   5.1 Development of the Brain

 

3. Define myelination during neural development.

 

ANS:

During this process, glia produce the insulating fatty sheaths that accelerate transmission in many vertebrate axons.

 

PTS:   1                    DIF:    factual           REF:   Maturation of the Vertebrate Brain

OBJ:   1                    TOP:   5.1 Development of the Brain

 

 

4. Describe how axons reach their targets during development.

 

ANS:

Axons follow the chemical gradient that is produced by the target cells.

 

PTS:   1                    DIF:    factual           REF:   Pathfinding by Axons

OBJ:   2                    TOP:   5.1 Development of the Brain

 

5. Define denervation supersensitivity.

 

ANS:

This is heightened sensitivity to a neurotransmitter after the destruction of an incoming axon.

 

PTS:   1                    DIF:    factual           REF:   Later Mechanisms of Recovery

OBJ:   2                    TOP:   5.2 Plasticity After Brain Damage

 

6. Describe how phantom limb sensations that seemingly come from a missing hand might occur when the face is touched.

 

ANS:

The area of the cortex that normally responds to the face could send collateral sprouts to the adjacent area of the cortex that was innervated by the hand.

 

PTS:   1                    DIF:    conceptual     REF:   Later Mechanisms of Recovery

OBJ:   2                    TOP:   5.2 Plasticity After Brain Damage

 

ESSAY

 

1. Describe the five main stages of growth and development of neurons.

 

ANS:

Answers will vary.

 

PTS:   1                    DIF:    factual           REF:   Maturation of the Vertebrate Brain

OBJ:   1                    TOP:   5.1 Development of the Brain

 

2. Describe how experience can alter brain development (give a specific example).

 

ANS:

Answers will vary.

 

PTS:   1                    DIF:    factual           REF:   Brain Damage and Short-term Recovery

OBJ:   1                    TOP:   5.2 Plasticity After Brain Damage

MSC:  www

 

3. Briefly describe how strokes affect the brain.

 

ANS:

Answers will vary.

 

PTS:   1                    DIF:    factual           REF:   Brain Damage and Short-term Recovery

OBJ:   1                    TOP:   5.2 Plasticity After Brain Damage

 

4. Briefly describe sprouting.

 

ANS:

Answers will vary.

 

PTS:   1                    DIF:    factual           REF:   Later Mechanisms of Recovery

OBJ:   2                    TOP:   5.2 Plasticity After Brain Damage

 

5. Describe the relationship of sensory representation and phantom limb sensation.

 

ANS:

Answers will vary.

 

PTS:   1                    DIF:    factual           REF:   Later Mechanisms of Recovery

OBJ:   2                    TOP:   5.2 Plasticity After Brain Damage

MSC:  www