Neuron Structure and Signal Propagation (3A)
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MCAT Biological and Biochemical Foundations of Living Systems › Neuron Structure and Signal Propagation (3A)
A lab compares conduction along two peripheral axons of equal diameter: Axon 1 is myelinated with long internodes and regularly spaced nodes of Ranvier; Axon 2 is unmyelinated. Both are stimulated with identical current injections at the axon initial segment, and both express similar densities of voltage-gated Na+ channels at spike initiation sites. Which factor most influences the speed of signal propagation in these neurons?
Myelination, which increases membrane resistance and decreases capacitance, allowing depolarization to spread farther between nodes before regeneration
Increased neurotransmitter packaging into synaptic vesicles at the axon terminal, which speeds action potential travel along the axon
Higher density of ligand-gated Na+ channels on dendrites, which increases the amplitude of graded potentials and therefore conduction velocity
A reversal of the normal direction of current flow such that action potentials move from axon terminals to soma more efficiently
Explanation
This question tests the understanding of neuron structure and signal propagation, focusing on factors influencing conduction velocity in myelinated versus unmyelinated axons. Myelination insulates axons, increasing membrane resistance and decreasing capacitance, which allows passive current spread over longer distances. In myelinated axons, this enables saltatory conduction where action potentials jump between nodes of Ranvier, speeding propagation. Choice B is consistent because myelination reduces current leak and capacitance, allowing faster depolarization spread in the myelinated axon. A distractor like choice A fails based on the misconception that ligand-gated channels directly affect axonal conduction velocity, whereas they primarily influence synaptic potentials. To apply to similar concepts, compare membrane properties like resistance and capacitance. Always confirm that myelination enhances speed without altering ion gradients directly.
In a study of demyelinating disease, an axon segment loses myelin but retains intact nodes of Ranvier. Recordings show that small depolarizations spread farther along the demyelinated region but decay more quickly in time, and some APs fail to propagate through the demyelinated zone. Which factor most influences the speed and reliability of signal propagation in this case?
Increased dendritic spine density in the demyelinated region increases synaptic input, which compensates for lost myelin and ensures reliable saltatory conduction.
Decreased extracellular Na$^+$ concentration in the demyelinated region increases the driving force for Na$^+$ entry, speeding propagation through the lesion.
Upregulation of ligand-gated receptors along the demyelinated axolemma replaces voltage-gated Na$^+$ channels, restoring AP propagation without affecting speed.
Increased membrane capacitance and decreased membrane resistance in the demyelinated region increase current leak and slow nodal depolarization, promoting conduction failure.
Explanation
This question tests understanding of how myelin affects passive membrane properties and action potential propagation. Myelin decreases membrane capacitance and increases membrane resistance, allowing depolarizing current to spread efficiently between nodes. Demyelination reverses these changes: increased capacitance requires more charge to depolarize the membrane, while decreased resistance allows more current to leak out. These changes slow the spread of depolarization and can cause conduction failure if the arriving current is insufficient to trigger the next node. The correct answer identifies these passive property changes as the key factor. Choice B incorrectly invokes dendritic spines on axons, while choice C wrongly suggests decreased extracellular Na+ (which would reduce, not increase, driving force). A critical principle is that myelin's effect on passive membrane properties, not active channel changes, determines conduction reliability in demyelinating conditions.
A pharmacologic agent selectively blocks AMPA-type glutamate receptors on a postsynaptic neuron but does not affect presynaptic APs or presynaptic Ca$^{2+}$ entry. After presynaptic stimulation, the postsynaptic neuron shows greatly reduced fast depolarizing responses, though slower responses mediated by metabotropic receptors remain. Based on these observations, which event occurs during synaptic transmission that is most consistent with the reduced fast response?
Neurotransmitter release is reduced because AMPA receptors normally repolarize the presynaptic terminal to terminate Ca$^{2+}$ influx.
Blocking AMPA receptors prevents AP propagation down the presynaptic axon because glutamate binding is required to open voltage-gated Na$^+$ channels.
Neurotransmitter release occurs normally, but blocking postsynaptic ligand-gated cation channels prevents rapid Na$^+$ influx that would generate a fast EPSP.
Blocking AMPA receptors prevents presynaptic vesicle docking because AMPA receptors serve as Ca$^{2+}$ channels on the presynaptic terminal.
Explanation
This question tests understanding of postsynaptic receptor function in synaptic transmission. AMPA receptors are ionotropic glutamate receptors that mediate fast excitatory postsynaptic potentials by allowing rapid Na+ (and K+) flux upon glutamate binding. Blocking these receptors prevents the fast depolarizing response while leaving presynaptic function intact, as evidenced by preserved metabotropic responses. The correct answer accurately describes normal neurotransmitter release with blocked postsynaptic reception. Choice B incorrectly assigns AMPA receptors to the presynaptic terminal, while choice C wrongly makes them necessary for axonal propagation. A key principle is that fast synaptic responses require functional postsynaptic ionotropic receptors, distinct from presynaptic release machinery or axonal conduction mechanisms.
An experiment increases extracellular K+ concentration while keeping extracellular Na+ constant. The resting membrane potential becomes less negative, and some neurons show reduced action potential amplitude. Which statement best describes the role of ion channels in action potential propagation that best accounts for the reduced amplitude?
Depolarized resting potential increases neurotransmitter release by opening postsynaptic ligand-gated Ca2+ channels, reducing spike amplitude
Higher extracellular K+ increases the Na+ electrochemical gradient, causing a larger Na+ influx and therefore smaller action potentials
Depolarized resting potential increases steady-state inactivation of voltage-gated Na+ channels, reducing available Na+ current during the upstroke
Higher extracellular K+ reverses axonal propagation so spikes travel from dendrites to soma, decreasing measured amplitude at the axon
Explanation
This question tests the understanding of neuron structure and signal propagation, focusing on resting potential and Na+ channel availability. Elevated extracellular K+ depolarizes rest, increasing Na+ channel inactivation via voltage dependence. This reduces available channels for upstroke, lowering spike amplitude. Choice D is consistent because inactivation decreases Na+ current, explaining reduced amplitude. A distractor like choice C fails based on the misconception that higher K+ boosts Na+ gradient, whereas it affects resting voltage. To check, plot inactivation curves. Recall that steady-state inactivation rises with depolarization.
A neuron’s axon collateral forms an axo-axonic synapse onto another neuron’s presynaptic terminal, where it increases Cl− conductance and reduces neurotransmitter release (presynaptic inhibition). Action potentials still invade the inhibited terminal. Based on this setup, which event occurs during synaptic transmission that best accounts for reduced release?
Increased presynaptic Cl− conductance reduces terminal depolarization and/or increases shunting, decreasing activation of voltage-gated Ca2+ channels needed for vesicle fusion
Increased presynaptic Cl− conductance reverses action potential direction so spikes no longer reach the terminal from the axon hillock
Increased presynaptic Cl− conductance directly blocks postsynaptic ligand-gated receptors, preventing neurotransmitter binding
Increased presynaptic Cl− conductance increases intracellular Na+ at rest, strengthening depolarization and decreasing Ca2+ influx
Explanation
This question tests the understanding of neuron structure and signal propagation, particularly presynaptic inhibition mechanisms. Increased Cl− conductance hyperpolarizes or shunts the terminal, reducing Ca2+ influx and release. This inhibits without blocking spike invasion. Choice A is consistent because shunting impairs Ca2+ activation. A distractor like choice B fails due to the misconception that presynaptic inputs directly block postsynaptic receptors. For inhibition types, differentiate sites. Note axo-axonic synapses modulate release.
In an experiment on unmyelinated axons, a segment is cooled while the rest remains at physiological temperature. Action potentials still propagate through the cooled segment but with delayed timing. Which factor most influences the speed of signal propagation in this condition?
Lower temperature reverses the direction of propagation so spikes move from axon terminal to soma, increasing transit time
Lower temperature slows voltage-gated channel kinetics, delaying activation/inactivation and thereby slowing conduction
Lower temperature increases extracellular Na+ concentration, which reduces the driving force for Na+ entry and speeds conduction
Lower temperature increases neurotransmitter receptor affinity at dendrites, which directly increases axonal conduction velocity
Explanation
This question tests the understanding of neuron structure and signal propagation, emphasizing temperature effects on channel kinetics. Lower temperature slows gating, delaying activation and conduction. This prolongs transit time. Choice C is consistent because kinetics slow overall propagation. A distractor like choice B fails due to the misconception that temperature alters concentrations, whereas it affects rates. For conditions, factor Q10 values. Note enzymes and channels are temperature-sensitive.
Two axons have the same diameter and myelination, but Axon A has shorter internode distances (more frequent nodes) than Axon B. Both have normal voltage-gated Na+ channel clustering at nodes. Which factor most influences the speed of signal propagation in these neurons?
Shorter internodes always increase conduction velocity because more nodes provide more Na+ channels to push current forward
Longer internodes (fewer nodes) generally increase conduction velocity by reducing the number of times the action potential must be regenerated, up to the point where internodes become too long for reliable depolarization
Internode distance reverses propagation direction by shifting spike initiation from the axon hillock to the axon terminal
Internode distance primarily changes neurotransmitter diffusion across the synaptic cleft, which determines axonal conduction velocity
Explanation
This question tests the understanding of neuron structure and signal propagation, focusing on internode length in saltatory conduction. Optimal internode length balances passive spread and regeneration frequency for maximal velocity. Longer internodes reduce regenerations but risk failure if too extended. Choice A is consistent because fewer nodes speed conduction up to a limit. A distractor like choice B fails due to the misconception that more nodes always accelerate, ignoring delay at each. For myelinated axons, optimize length constants. Confirm velocity peaks at intermediate internodes.
An experiment compares two populations of peripheral motor axons: Population 1 has normal myelination; Population 2 has reduced myelin thickness but unchanged axon diameter and normal resting ion gradients. In both groups, voltage-gated Na+ channels remain clustered at nodes of Ranvier. When identical suprathreshold stimuli are applied proximally, which factor most influences the expected difference in signal propagation speed between the two populations?
Reduced myelin causes action potentials to initiate in dendrites rather than the axon initial segment, increasing conduction distance.
Reduced myelin shifts the Na+ equilibrium potential to more negative values, slowing depolarization at the axon hillock.
Reduced myelin increases membrane capacitance and current leak across internodes, slowing the rate at which downstream nodes reach threshold.
Reduced myelin increases neurotransmitter release probability at the neuromuscular junction, slowing axonal conduction.
Explanation
This question tests understanding of how myelin thickness affects conduction velocity in saltatory conduction. Myelin acts as an insulator that reduces membrane capacitance and prevents current leak across internodes, allowing depolarizing current to travel efficiently between nodes. When myelin is thinner, the membrane capacitance increases and more current leaks out across the internode, reducing the amount of depolarizing current that reaches the next node and slowing the rate at which it reaches threshold. The correct answer D accurately describes this mechanism of reduced conduction velocity. Answer B incorrectly introduces neurotransmitter release, which occurs at synapses, not along the axon during conduction. The fundamental principle is that myelin thickness directly affects the passive electrical properties of the axon, with thicker myelin providing better insulation and faster conduction.
At an excitatory synapse, neurotransmitter binds ionotropic receptors permeable to Na+ and K+. In a modified condition, the postsynaptic neuron is experimentally clamped near the Na+ equilibrium potential while presynaptic release remains unchanged. Compared with baseline, the postsynaptic response to the same neurotransmitter release is smaller. Which statement best accounts for this observation in terms of signal propagation principles?
The EPSP is smaller because action potentials normally propagate from dendrites to soma only when Na+ is higher inside than outside.
The EPSP is smaller because voltage-gated Na+ channels at the presynaptic terminal require postsynaptic depolarization to open and release vesicles.
Clamping near the Na+ equilibrium potential increases Na+ influx, which hyperpolarizes the postsynaptic neuron and reduces transmitter binding.
Driving force for Na+ entry is reduced near the Na+ equilibrium potential, decreasing net inward current through the receptor and thus reducing the EPSP.
Explanation
This question tests understanding of driving force and synaptic current generation. Ionotropic receptors permeable to Na+ and K+ generate EPSPs through net inward current, primarily carried by Na+ influx down its electrochemical gradient. When the postsynaptic membrane is clamped near the Na+ equilibrium potential (~+60 mV), the driving force for Na+ entry (Vm - ENa) approaches zero, dramatically reducing Na+ influx through open receptors. The correct answer D correctly identifies that reduced driving force for Na+ decreases the net inward current and thus the EPSP amplitude. Answer B incorrectly claims that being near ENa increases Na+ influx, when the opposite is true. A critical principle for synaptic physiology is that current through an ion channel depends on both conductance (number of open channels) and driving force (difference between membrane potential and equilibrium potential).
At a chemical synapse, a presynaptic action potential arrives at an axon terminal. In one condition, extracellular Ca2+ at the terminal is acutely reduced while Na+ and K+ gradients are unchanged. Postsynaptic recordings show markedly smaller excitatory postsynaptic potentials (EPSPs) despite normal presynaptic action potential amplitude. Based on principles of synaptic transmission, which event is most directly reduced by lowering extracellular Ca2+?
Propagation of the presynaptic action potential due to reduced saltatory conduction across the presynaptic dendrites.
Opening of postsynaptic ligand-gated cation channels due to decreased postsynaptic depolarization at the axon hillock.
Vesicle fusion with the presynaptic membrane due to reduced Ca2+-triggered exocytosis following terminal depolarization.
Resting membrane potential of the postsynaptic neuron due to decreased Na+ concentration outside the cell.
Explanation
This question tests understanding of calcium's role in synaptic transmission. When an action potential reaches the presynaptic terminal, voltage-gated Ca2+ channels open, allowing calcium influx that triggers vesicle fusion and neurotransmitter release. Reducing extracellular Ca2+ directly reduces this calcium influx, leading to less vesicle fusion and smaller postsynaptic responses. The correct answer B accurately identifies that Ca2+-triggered exocytosis (vesicle fusion) is the process most directly affected by low extracellular calcium. Answer A incorrectly focuses on postsynaptic events, but the question states the presynaptic action potential is normal, indicating the effect is presynaptic. The key principle is that calcium couples electrical signaling (action potential arrival) to chemical signaling (neurotransmitter release) at synapses.