Chapter 3: Synapses and Synaptic Transmission

Chapter 3: Synapses and Synaptic Transmission

Complete Chapter Questions With Answers

Sample Questions Are Posted Below

1. The second messenger in a second messenger system is a(n):
2. G-protein
3. α chain of the G-protein
4. Enzyme inside the neuron that can trigger responses within the neuron
5. Neurotransmitter
6. Gene

ANS: C

Rationale: The G-protein–mediated second-messenger system involves: (1) binding of a neurotransmitter (first messenger) to a G-protein–associated membrane receptor; (2) activation of an effector enzyme (second messenger); (3) increased levels of the second messenger that elicits responses within the neuron.

2. Second messengers may initiate the:
3. Opening of membrane ion channels
4. Activation of genes, causing increased synthesis of specific cellular products
5. Modulation of Ca⁺² levels inside the cell
6. A, B, and C
7. None of the above

ANS: D

Rationale: Second messengers activate responses inside the cell. In these cases, a single neurotransmitter might turn on a molecular pathway that ends with a change in gene expression, the opening of ion channels, and/or phosphorylation of a structural protein.

3. Which one of the following can serve as the postsynaptic cell of a synapse?
4. Smooth muscle cell in an artery
5. Hepatocyte in the liver
6. Neuron in the thalamus
7. Muscle cell in the triceps
8. All of the above

ANS: E

Rationale: A postsynaptic cell is any cell of an organ, gland, blood vessel, neuron, or muscle cell that synapses with a neuron.

4. ACh receptor subtypes include:
5. Adrenergic and noradrenergic
6. Nicotinic and muscarinic
7. Alpha and beta
8. Alpha and gamma
9. None of the above

ANS: B

Rationale: Receptors that bind ACh fall into two categories: nicotinic and muscarinic. These receptors are distinguished by their ability to bind certain drugs. Nicotine, derived from tobacco, selectively activates the nicotinic receptors. Muscarine, a poison derived from mushrooms, activates only the muscarinic receptors.

5. How does onabotulinumtoxinA (BOTOX) therapeutically produce paresis in overactive muscles?
6. Acts as an antagonist by binding to the ACh receptor on the postsynaptic membrane.
7. Rapidly degrades ACh in the synaptic cleft.
8. Facilitates the reuptake and sequestration of ACh into the presynaptic cell.
9. Disrupts the protein structure of the muscle cell receptor, thus preventing ACh from binding.
10. Inhibits the release of ACh from the presynaptic terminal at the neuromuscular junction.

ANS: E

Rationale: Botulinum toxin is naturally produced by a family of bacteria and, when ingested, causes widespread paralysis by inhibiting the release of ACh at the neuromuscular junction. When small doses of BOTOX are therapeutically injected directly into an overactive muscle, the inhibition of ACh release reduces or prevents contraction of the injected muscle.