Free MCAT-style practice, 3A
MCAT Action Potential and Synaptic Transmission Practice Questions
Eight free MCAT-style practice questions on action potential phases, refractory periods, myelination, synaptic transmission, neurotransmitters, summation, the autonomic nervous system and reflexes, with explanations.
Quick concept primer
An action potential is an all-or-none event. A graded depolarization that reaches threshold (about -55 mV) opens voltage-gated Na+ channels, producing the rising phase. Na+ channels then inactivate and voltage-gated K+ channels open, repolarizing the membrane and sometimes overshooting to a brief hyperpolarization. The absolute refractory period reflects inactivated Na+ channels and ensures the impulse travels in one direction. Myelin speeds conduction by forcing the current to jump between nodes of Ranvier (saltatory conduction).
At the synapse, an action potential opens voltage-gated Ca2+ channels, Ca2+ entry triggers SNARE-mediated vesicle fusion, and neurotransmitter diffuses across the cleft to ionotropic or metabotropic receptors. Postsynaptic potentials sum in space and time at the axon hillock. The autonomic nervous system uses acetylcholine at all preganglionic synapses, acetylcholine on muscarinic receptors in parasympathetic targets, and mainly norepinephrine at sympathetic targets.
Traps: a stronger stimulus makes more frequent action potentials, not larger ones; and a toxin that blocks Na+ channels leaves the resting potential intact.
8 practice questions
Question 1
Tetrodotoxin blocks voltage-gated Na+ channels. When applied to a nerve axon, which effect is expected?
- Action potentials fail to be generated, while the resting membrane potential is largely unchanged
- The resting membrane potential collapses to 0 mV
- Action potentials become larger
- The refractory period disappears
Show answer and explanation
Answer: A. Action potentials fail to be generated, while the resting membrane potential is largely unchanged
The resting potential depends mainly on K+ leak channels, so blocking the voltage-gated Na+ channels barely changes it. Without those channels, a depolarizing stimulus cannot trigger the regenerative Na+ influx of the rising phase, and no action potential occurs. Local anesthetics such as lidocaine work by a similar mechanism.
Question 2
Axons were compared for conduction velocity.
| Axon | Diameter (micrometers) | Myelination | Conduction velocity (m/s) |
|---|---|---|---|
| W | 1 | no | 1 |
| X | 4 | no | 2 |
| Y | 4 | yes | 25 |
| Z | 15 | yes | 90 |
Which comparison most directly isolates the effect of myelin?
- X compared with Y
- Y compared with Z
- W compared with Z
- W compared with X
Show answer and explanation
Answer: A. X compared with Y
To isolate one variable, compare axons that differ only in that variable. X and Y have the same diameter (4 micrometers) but differ in myelination, and myelination increases velocity roughly twelvefold (2 to 25 m/s). W and X differ only in diameter, Y and Z differ only in diameter, and W and Z differ in both.
Question 3
A patient has multiple sclerosis. Which cell type is damaged, and what is the consequence for conduction?
- Astrocytes; the blood-brain barrier is unaffected
- Microglia; conduction velocity increases
- Oligodendrocytes; loss of myelin in the CNS slows or blocks conduction
- Schwann cells; conduction fails in the peripheral nervous system only
Show answer and explanation
Answer: C. Oligodendrocytes; loss of myelin in the CNS slows or blocks conduction
Multiple sclerosis is an autoimmune attack on CNS myelin, which is produced by oligodendrocytes (one oligodendrocyte myelinates several axon segments). Demyelination makes current leak through the exposed membrane, slowing or blocking saltatory conduction. Schwann cells myelinate peripheral axons, and their damage is seen in conditions such as Guillain-Barre syndrome.
Question 4
Botulinum toxin cleaves SNARE proteins in the presynaptic terminal of motor neurons. What is the expected clinical effect?
- Loss of sensation only
- Flaccid paralysis from failure of acetylcholine release despite normal action potentials in the nerve
- Increased muscle tone
- Spastic paralysis from excess acetylcholine release
Show answer and explanation
Answer: B. Flaccid paralysis from failure of acetylcholine release despite normal action potentials in the nerve
SNARE proteins mediate fusion of synaptic vesicles with the presynaptic membrane after Ca2+ entry. When they are cleaved, acetylcholine is not released at the neuromuscular junction, so the muscle receives no signal and becomes limp. The action potential in the axon is normal, but the signal is not transmitted across the synapse.
Question 5
Activation of a GABA-A receptor on a mature neuron, where E(Cl) is about -65 mV and the resting potential is -60 mV, typically causes
- Ca2+ influx and neurotransmitter release
- Na+ influx and depolarization
- K+ efflux and no change in membrane potential
- Cl- influx and hyperpolarization toward E(Cl), making the cell less likely to fire
Show answer and explanation
Answer: D. Cl- influx and hyperpolarization toward E(Cl), making the cell less likely to fire
The GABA-A receptor is a ligand-gated Cl- channel. When it opens, Cl- moves in the direction that shifts the membrane toward E(Cl). Since E(Cl) is more negative than the resting potential here, Cl- enters and the neuron hyperpolarizes (and the increased conductance also shunts excitatory current). Benzodiazepines enhance this effect, which accounts for their sedative action.
Question 6
A neuron has a resting potential of -70 mV and a threshold of -55 mV. Each EPSP depolarizes the membrane by 5 mV, and each IPSP hyperpolarizes it by 5 mV at the axon hillock. Assuming linear summation, how many EPSPs must arrive simultaneously to reach threshold if one IPSP arrives at the same time?
- 3
- 4
- 5
- 6
Show answer and explanation
Answer: B. 4
The membrane must depolarize by 15 mV. One IPSP contributes -5 mV, so the EPSPs must supply 20 mV in total, which is 4 EPSPs at 5 mV each (net +15 mV). Without the IPSP, 3 EPSPs would suffice. This illustrates how inhibitory input offsets excitatory input through summation at the axon hillock.
Question 7
A patient is given atropine, a muscarinic receptor antagonist. Which set of effects is most expected?
- Pupil constriction and increased heart rate
- Pupil dilation, increased heart rate and dry mouth
- Pupil constriction, slowed heart rate and increased salivation
- Bronchoconstriction and increased gut motility
Show answer and explanation
Answer: B. Pupil dilation, increased heart rate and dry mouth
Muscarinic receptors mediate the effects of the parasympathetic postganglionic neurons. Blocking them removes parasympathetic tone: the pupil dilates, the heart speeds up (loss of vagal slowing), salivation decreases and gut motility falls. The drug does not block nicotinic receptors, so the sympathetic and parasympathetic ganglia still transmit.
Question 8
In the knee-jerk (patellar tendon stretch) reflex, which of the following is true?
- Sensory neurons synapse directly onto motor neurons in the spinal cord, and the sensory axon enters through the dorsal root while the motor axon exits through the ventral root
- The sensory neuron exits through the ventral root
- The reflex arc requires processing in the cerebral cortex
- The reflex includes at least three interneurons in series
Show answer and explanation
Answer: A. Sensory neurons synapse directly onto motor neurons in the spinal cord, and the sensory axon enters through the dorsal root while the motor axon exits through the ventral root
The stretch reflex is monosynaptic: the sensory neuron from the muscle spindle synapses directly on the alpha motor neuron of the same muscle, which is why the latency is so short. Sensory (afferent) fibers enter the cord through the dorsal root and motor (efferent) fibers leave through the ventral root. The cortex is informed but is not needed for the reflex.