Nervous System Organization and Function (3A)
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MCAT Biological and Biochemical Foundations of Living Systems › Nervous System Organization and Function (3A)
A neuron receives two simultaneous synaptic inputs: an excitatory synapse on a distal dendrite and an inhibitory synapse located on the soma near the axon hillock. Both synapses are activated at the same time with equal transmitter release probability. The inhibitory receptor is a ligand-gated Cl$^-$ channel whose reversal potential is near the resting membrane potential. Based on the scenario, which function is most consistent with the somatic inhibitory synapse?
Assume: action potentials initiate at the axon hillock when local depolarization reaches threshold.
It triggers firing by opening Cl$^-$ channels that depolarize the membrane above threshold at the soma
It reduces the likelihood of firing by shunting depolarizing current near the hillock, limiting the excitatory input’s effect on threshold
It reduces firing only by decreasing acetylcholine secretion into the bloodstream, lowering global neuronal excitability
It increases the likelihood of firing by summating with the distal excitatory input to depolarize the hillock
Explanation
This question tests understanding of shunting inhibition and synaptic integration at the axon hillock. When an inhibitory synapse opens Cl- channels near the axon hillock, it creates a low-resistance pathway (shunt) that diverts depolarizing current from reaching threshold at the spike initiation zone. Even though the Cl- reversal potential is near rest (not hyperpolarizing), the increased conductance reduces the effectiveness of excitatory inputs by providing an alternate current path. The correct answer (B) recognizes this shunting mechanism where somatic inhibition strategically positioned near the hillock can veto distal excitation. Answer A incorrectly suggests inhibition would summate with excitation to promote firing, missing the shunting effect. When analyzing synaptic integration, consider both the location of inputs and the conductance changes, not just the reversal potentials.
A cultured excitatory synapse was voltage-clamped at the postsynaptic neuron. The presynaptic terminal was stimulated with a single action potential. Under control conditions, a fast postsynaptic current (PSC) is recorded. When extracellular Ca$^{2+}$ is reduced from 2 mM to 0.2 mM (Mg$^{2+}$ unchanged), the PSC amplitude decreases markedly, while presynaptic action potential shape is unchanged.
Which mechanism best explains the reduced PSC amplitude?
(Assume the same number of postsynaptic receptors are present and the neurotransmitter is cleared normally.)
Reduced Ca$^{2+}$ directly blocks postsynaptic ligand-gated channels, preventing neurotransmitter binding
Reduced Ca$^{2+}$ increases the driving force for Na$^+$ influx through postsynaptic receptors, decreasing PSC amplitude
Reduced Ca$^{2+}$ converts neurotransmitter release into endocrine signaling, delaying PSCs beyond the recording window
Reduced Ca$^{2+}$ entry decreases synaptic vesicle fusion probability, lowering neurotransmitter release per presynaptic spike
Explanation
This question tests understanding of synaptic transmission mechanisms in the nervous system. Neurotransmitter release at chemical synapses is triggered by calcium influx through voltage-gated channels, promoting vesicle fusion. Reducing extracellular calcium limits this influx, decreasing the probability of vesicle release without altering presynaptic action potentials. The correct answer aligns because lower calcium entry reduces fusion events, leading to smaller postsynaptic currents from less neurotransmitter. A common distractor like option B fails by misunderstanding that reduced calcium affects presynaptic release, not postsynaptic driving forces for sodium. For similar questions, confirm if the manipulation targets presynaptic calcium-dependent processes. Remember that postsynaptic currents depend on quantal release modulated by calcium levels.
In a sensory pathway, a peripheral mechanoreceptor afferent synapses onto a second-order neuron in the spinal cord. The second-order neuron then projects to the thalamus. In a lesion experiment, the synapse between the afferent and the second-order neuron is pharmacologically silenced, but the second-order neuron and its axon remain intact and excitable. Mechanical stimulation of the skin still generates action potentials in the afferent.
What outcome would be expected in the thalamic neuron that normally receives input from the second-order neuron during skin stimulation?
Unchanged stimulus-evoked activity because action potentials in the afferent propagate directly to the thalamus
Increased stimulus-evoked activity because silencing the synapse removes refractory periods in the afferent
Delayed stimulus-evoked activity because the signal is rerouted through endocrine circulation to reach the thalamus
Reduced or absent stimulus-evoked activity because the second-order neuron is no longer driven by afferent synaptic input
Explanation
This question tests understanding of neural pathway organization in the nervous system. Sensory pathways rely on synaptic transmission to relay signals through second-order neurons to higher centers. Silencing the synapse isolates the second-order neuron, preventing afferent-driven activity. The correct answer aligns because without synaptic input, the thalamic response to stimulation is lost. A common distractor like option B fails by misunderstanding that blocking removes excitation, not refractory constraints. For similar questions, trace signal flow through synapses. Confirm that pathway disruptions abolish downstream activity if synaptic drive is essential.
At a glutamatergic synapse, an investigator measures miniature excitatory postsynaptic currents (mEPSCs) in the postsynaptic neuron in the presence of tetrodotoxin to block presynaptic action potentials. A drug is applied that decreases the number of functional postsynaptic receptors without affecting presynaptic vesicle fusion.
Which change is most consistent with the drug’s effect on the mEPSCs?
No change in mEPSCs because receptor changes affect only endocrine signaling, not synaptic currents
Decreased mEPSC amplitude with unchanged mEPSC frequency
Decreased mEPSC frequency with unchanged mEPSC amplitude
Increased mEPSC frequency because fewer receptors increase presynaptic release probability
Explanation
This question tests understanding of quantal synaptic transmission in the nervous system. Miniature EPSCs reflect single vesicle releases, with amplitude depending on postsynaptic receptor density. Reducing receptors decreases current per vesicle without affecting spontaneous release frequency. The correct answer aligns because amplitude drops while frequency remains unchanged. A common distractor like option B fails by misunderstanding that postsynaptic changes do not alter presynaptic fusion rates. For similar questions, differentiate quantal size from release probability. Confirm that mEPSC amplitude probes postsynaptic sensitivity.
A postsynaptic neuron is voltage-clamped at $-70$ mV. Activation of a ligand-gated cation channel produces an inward current. When the membrane is clamped at 0 mV, activation of the same channel produces ~0 net current. The channel is permeable to Na$^+$ and K$^+$.
Which mechanism best explains the near-zero current at 0 mV?
At 0 mV Na$^+$ and K$^+$ concentrations become equal across the membrane, eliminating driving force
At 0 mV the membrane potential is near the channel’s reversal potential, so Na$^+$ influx and K$^+$ efflux balance to yield minimal net current
At 0 mV the channel becomes permanently inactivated, preventing ion flow regardless of ligand binding
At 0 mV the neurotransmitter is converted into a hormone that cannot open ion channels
Explanation
This question tests understanding of ion channel reversal potentials in synaptic signaling. Non-selective cation channels have reversal potentials near 0 mV, balancing sodium influx and potassium efflux. At 0 mV, driving forces equalize, yielding zero net current. The correct answer aligns because clamping at reversal eliminates current flow. A common distractor like option B fails by misunderstanding that ligand-gated channels do not inactivate like voltage-gated ones. For similar questions, calculate reversal using permeabilities. Confirm that current direction reverses around Erev in voltage-clamp.
A neuron is stimulated repeatedly with identical depolarizing current pulses. In one condition, extracellular K$^+$ is increased modestly (with extracellular Na$^+$ unchanged). The resting membrane potential becomes less negative, and the neuron initially fires more easily, but during sustained stimulation it begins to fail to generate action potentials.
Which mechanism best explains the failure to fire during sustained stimulation in elevated extracellular K$^+$?
Elevated extracellular K$^+$ increases the Na$^+$ equilibrium potential, eliminating the action potential upstroke
Chronic depolarization promotes voltage-gated Na$^+$ channel inactivation, reducing available channels for action potential initiation
Elevated extracellular K$^+$ triggers endocrine release of K$^+$ from glia, which blocks action potentials
Elevated extracellular K$^+$ hyperpolarizes the membrane, preventing Na$^+$ channel activation
Explanation
This question tests understanding of ion effects on neuronal excitability in the nervous system. Elevated extracellular potassium depolarizes rest potential, initially easing firing but promoting sodium inactivation during sustained activity. Chronic depolarization inactivates channels, causing failures. The correct answer aligns because fewer available channels impair AP generation. A common distractor like option B fails by misunderstanding that high potassium depolarizes, not hyperpolarizes. For similar questions, consider Nernst potential shifts. Confirm that accommodation arises from inactivation in depolarized states.
In a simple neural pathway, two excitatory presynaptic neurons (P1 and P2) converge onto a postsynaptic neuron (N). P1 and P2 each produce a subthreshold EPSP in N when stimulated alone. When P1 and P2 are stimulated simultaneously, N reaches threshold and fires an action potential.
Which mechanism best explains N firing only during simultaneous stimulation?
Spatial summation of EPSPs increases net depolarization at the axon initial segment to reach threshold
Simultaneous stimulation depletes neurotransmitter, increasing postsynaptic depolarization
Simultaneous stimulation releases neurotransmitter into blood, allowing endocrine summation to trigger firing
Simultaneous stimulation causes Na$^+$ channel inactivation to reverse, lowering depolarization and triggering firing
Explanation
This question tests understanding of synaptic summation in neuronal integration. Spatial summation combines subthreshold EPSPs from multiple inputs to reach firing threshold. Simultaneous activation sums depolarizations axially. The correct answer aligns because net depolarization triggers the AP. A common distractor like option B fails by misunderstanding that summation adds, not reverses, inactivation. For similar questions, distinguish spatial from temporal summation. Confirm that convergent inputs enable threshold crossing via addition.
A neuron is exposed to a toxin that selectively blocks voltage-gated Ca$^{2+}$ channels in presynaptic terminals but does not affect voltage-gated Na$^+$ channels along the axon. Presynaptic action potentials still invade the terminal normally.
Based on the scenario, which function is most consistent with the toxin’s effect on synaptic transmission?
Increased neurotransmitter release because Ca$^{2+}$ influx normally inhibits vesicle fusion
Unchanged neurotransmitter release because Na$^+$ entry at the terminal is sufficient to fuse vesicles
Reduced neurotransmitter release because Ca$^{2+}$ influx is required to trigger synaptic vesicle fusion
Faster neurotransmitter diffusion because Ca$^{2+}$ channels regulate synaptic cleft width like a hormone
Explanation
This question tests understanding of calcium's role in synaptic release in the nervous system. Presynaptic calcium influx is essential for vesicle fusion and neurotransmitter exocytosis. Blocking calcium channels impairs release despite normal action potential invasion. The correct answer aligns because absent calcium entry halts transmission. A common distractor like option B fails by misunderstanding that calcium triggers, not inhibits, fusion. For similar questions, identify calcium-dependent steps in neurotransmission. Verify that axonal conduction persists but terminal release fails without calcium.
In a neuron, voltage-gated Na$^+$ channels open rapidly when the membrane is depolarized to threshold, producing the rising phase of the action potential. An experimental mutation slows Na$^+$ channel inactivation but does not alter activation threshold. When a brief depolarizing current is injected, the neuron produces an action potential with a prolonged depolarized phase.
Which mechanism best explains the prolonged depolarization?
Delayed Na$^+$ channel inactivation sustains inward Na$^+$ current, opposing repolarization
Delayed Na$^+$ channel inactivation increases Cl$^-$ influx, prolonging depolarization
Delayed Na$^+$ channel inactivation reduces Na$^+$ influx, accelerating repolarization
Delayed Na$^+$ channel inactivation triggers neurotransmitter release into blood, prolonging depolarization via hormones
Explanation
This question tests understanding of action potential duration control in the nervous system. Sodium channel inactivation terminates inward current, allowing repolarization via potassium efflux. Slowing inactivation sustains sodium influx, prolonging the depolarized phase. The correct answer aligns because persistent current opposes repolarization, extending the plateau. A common distractor like option B fails by misunderstanding that delayed inactivation prolongs, not reduces, depolarization. For similar questions, examine channel kinetics in AP phases. Verify that inactivation defects lead to extended APs in channelopathies.
In a patch-clamp experiment on a neuron, an investigator injects a constant depolarizing current step. Under control conditions, the neuron fires an action potential. After applying a drug that selectively prolongs the open time of voltage-gated K$^+$ channels during the falling phase of the action potential, the neuron still fires but the action potential is narrower and the after-hyperpolarization is larger.
Which mechanism best explains these changes in action potential shape?
Prolonged K$^+$ channel opening increases neurotransmitter release from the soma, narrowing the spike via hormonal feedback
Prolonged K$^+$ channel opening raises intracellular K$^+$ enough to reverse the K$^+$ gradient, decreasing after-hyperpolarization
Enhanced K$^+$ efflux accelerates repolarization and deepens after-hyperpolarization by driving $V_m$ toward $E_K$
Enhanced K$^+$ efflux slows repolarization by preventing Na$^+$ channel inactivation, widening the spike
Explanation
This question tests understanding of action potential repolarization in the nervous system. Voltage-gated potassium channels facilitate repolarization by allowing potassium efflux, restoring membrane potential to rest. Prolonging their open time enhances efflux, speeding repolarization and deepening after-hyperpolarization. The correct answer aligns because increased potassium conductance narrows the spike and amplifies hyperpolarization toward EK. A common distractor like option B fails by misunderstanding that enhanced potassium efflux accelerates, not slows, repolarization. For similar questions, analyze ion currents during AP phases. Verify that potassium modulation affects falling phase duration and refractory properties.