- Which of the following best explains why this demyelination impairs nerve impulse transmission, leading to symptoms like muscle weakness and poor coordination?
Answer: The absence of myelin allows local currents to dissipate, preventing the membrane at the next node of Ranvier from reaching threshold potential.
Myelin acts as an electrical insulator, preventing ion leakage across the axon membrane. This allows the local current generated during an action potential to travel further and faster to the next node of Ranvier, triggering depolarization there. Without myelin, this current dissipates, and the signal may not be strong enough to reach threshold at the next node, effectively blocking propagation. The other options describe effects on the synapse (B, D) or resting potential (C) that are not the primary consequence of demyelination.
- Action potentials are 'all-or-nothing' events of a fixed amplitude. How, then, does the nervous system encode information about the intensity of a stimulus, such as distinguishing a dim light from a bright light?
Answer: By increasing the frequency of action potentials fired per unit of time for stronger stimuli.
The nervous system uses frequency modulation to encode stimulus intensity. A stronger stimulus (like a bright light) will cause a sensory neuron to fire action potentials at a higher rate (more potentials per second) than a weaker stimulus (a dim light). The amplitude and speed of each individual action potential remain constant for a given neuron. This change in frequency is interpreted by the central nervous system as a change in stimulus intensity.
- An action potential propagates along an axon as a wave of depolarization. What is the immediate cause of the depolarization of the membrane segment just ahead of the advancing action potential?
Answer: The diffusion of Na+ ions along the inside of the axon from the adjacent depolarized region, creating a local current.
When one segment of the axon depolarizes due to Na+ influx, these positive ions diffuse laterally inside the axon. This movement of charge, known as a local current, depolarizes the adjacent segment of the membrane to its threshold potential. This triggers the opening of voltage-gated Na+ channels in that new segment, continuing the propagation of the action potential. Neurotransmitters are at synapses (A), the pump works against this process (B), and K+ channel opening causes repolarization (D).
- Which structural feature of a chemical synapse is most directly responsible for ensuring that nerve impulses are transmitted in only one direction, from the presynaptic to the postsynaptic neuron?
Answer: The location of synaptic vesicles in the presynaptic terminal and receptors on the postsynaptic membrane.
Unidirectional flow is guaranteed by the physical separation of the signal-releasing machinery and the signal-receiving machinery. Neurotransmitters are stored in vesicles and released from the presynaptic terminal. The specific protein receptors that bind these neurotransmitters are embedded in the membrane of the postsynaptic neuron. There are no vesicles on the postsynaptic side and no receptors on the presynaptic side, so the signal can only travel in one direction across the cleft. The refractory period (D) ensures unidirectional flow along an axon, not across a synapse.
- In many real reflex arcs, a relay neuron (interneuron) is located between the sensory and motor neuron. What is a primary functional advantage of including a relay neuron in the circuit?
Answer: It allows for the integration of signals, such as inhibiting an opposing muscle group during the reflex.
Relay neurons allow for more complex processing within the spinal cord. A single sensory neuron can synapse with multiple relay neurons. One relay neuron might excite the flexor motor neuron (to pull the hand away), while another, inhibitory, relay neuron synapses with the motor neuron for the opposing extensor muscle, causing it to relax. This coordination of opposing muscles (reciprocal inhibition) makes the reflex more efficient and is a key role of interneurons. A is incorrect as reflexes are fast and subconscious. C is incorrect. D is incorrect as the sensory-motor synapse is also chemical.
- The resting potential of a neuron (around -70 mV) is primarily established by the differential permeability of the membrane to certain ions. Which statement most accurately describes this situation? (HL Content)
Answer: The membrane is slightly permeable to Na+ and highly permeable to K+, allowing K+ to leak out down its concentration gradient, making the inside negative.
The resting potential is primarily due to potassium leak channels, which make the membrane much more permeable to K+ than to other ions like Na+. Since the concentration of K+ is high inside the cell, K+ ions diffuse out down their concentration gradient, taking positive charge with them. This leaves the inside of the cell with a net negative charge. The Na+/K+ pump maintains these gradients but the potential itself is set by the K+ diffusion through leak channels. Choice C would result in a positive resting potential. Choices B and D misrepresent the role of permeability.
- The absolute refractory period is a brief time following an action potential when a second action potential cannot be initiated, regardless of stimulus strength. What is the primary molecular mechanism responsible for this period?
Answer: The voltage-gated Na+ channels are in an inactivated state and cannot be opened by depolarization.
During the absolute refractory period, the voltage-gated sodium channels have a component (the inactivation gate) that plugs the channel pore. This gate remains closed until the membrane repolarizes. While in this inactivated state, the channel cannot open again, even if the membrane is depolarized. This is the key reason a new action potential cannot be started. Choice A describes the relative refractory period. Choice B is incorrect as the pump is slow and many action potentials can fire before gradients run down. Choice D relates to synaptic transmission, not the properties of the axon membrane itself.
- The venom of the funnel-web spider contains a toxin that blocks voltage-gated calcium channels in the presynaptic terminals of neurons. What would be the most direct consequence of this venom on a chemical synapse?
Answer: The presynaptic terminal would be unable to release neurotransmitters into the synaptic cleft.
The arrival of an action potential at the presynaptic terminal opens voltage-gated Ca2+ channels. The subsequent influx of Ca2+ is the critical trigger for the fusion of synaptic vesicles with the presynaptic membrane and the release of neurotransmitters. By blocking these Ca2+ channels, the toxin prevents this trigger, thus blocking neurotransmitter release and synaptic transmission. The action potential itself can still reach the terminal (A), and the toxin does not affect reuptake (B) or receptor binding (D).
- A local anesthetic such as lidocaine works by blocking voltage-gated sodium channels. Why does this action prevent the sensation of pain?
Answer: It prevents sensory neurons from generating and propagating action potentials to the central nervous system.
The sensation of pain is transmitted to the brain via action potentials in sensory neurons. Lidocaine blocks the voltage-gated sodium channels that are essential for the depolarization phase of an action potential. Without functioning sodium channels, the neuron cannot fire an action potential, even if it is stimulated by a painful event. Therefore, the pain signal is never generated or propagated to the brain. While it does prevent neurotransmitter release (C), this is a downstream consequence of blocking the action potential itself (A), which is the primary mechanism.
- Following the repolarization phase of an action potential, the membrane potential often briefly becomes more negative than the resting potential. What is the direct cause of this hyperpolarization, or 'undershoot'?
Answer: The voltage-gated potassium channels being slow to close, allowing continued efflux of K+ ions.
The hyperpolarization phase occurs because the voltage-gated K+ channels that opened during repolarization are slower to close than the voltage-gated Na+ channels are to inactivate. This means that for a brief period, the membrane's permeability to K+ is even higher than it is at rest. The continued efflux of positive K+ ions drives the membrane potential closer to the K+ equilibrium potential, which is more negative than the resting potential.
- Curare is a plant-derived toxin that acts as a competitive antagonist at nicotinic acetylcholine receptors on the motor end plate of skeletal muscle cells. What is the direct physiological effect of curare poisoning?
Answer: It blocks the action of acetylcholine, preventing depolarization of the muscle fiber and causing flaccid paralysis.
As a competitive antagonist, curare binds to the acetylcholine receptors without activating them. This physically blocks acetylcholine from binding. Without acetylcholine binding, the ligand-gated ion channels on the muscle cell membrane do not open, preventing depolarization and subsequent muscle contraction. This results in muscle weakness and flaccid paralysis. Choice A describes an agonist. Choices B and D describe toxins that act on the presynaptic terminal or on enzymes in the cleft, respectively, not the postsynaptic receptor.
- How does the binding of GABA to a postsynaptic GABAA receptor typically prevent the postsynaptic neuron from firing an action potential? (HL Content)
Answer: It opens ligand-gated Cl- channels, causing an influx of negative ions and hyperpolarization (an IPSP).
GABAA receptors are ligand-gated chloride ion channels. When GABA binds, the channel opens, allowing negatively charged chloride ions (Cl-) to flow into the cell. This influx of negative charge makes the inside of the membrane more negative, a process called hyperpolarization. This creates an inhibitory postsynaptic potential (IPSP), which moves the membrane potential further away from the threshold, making it less likely to fire an action potential. The other options describe excitatory or unrelated mechanisms.
- During the repolarization phase of an action potential, what is the state of the primary voltage-gated ion channels involved in generating the potential?
Answer: Voltage-gated Na+ channels are inactivated, while voltage-gated K+ channels are open.
Repolarization is caused by the closing and inactivation of voltage-gated Na+ channels and the opening of voltage-gated K+ channels. The efflux of K+ ions out of the cell makes the membrane potential negative again. Choice A describes depolarization. Choice C is incorrect because K+ channels are open. Choice D is incorrect because Na+ channels are inactivated, not open, during repolarization.
- Considering the factors that influence the speed of nerve impulse conduction, which of the following neurons would transmit an action potential the fastest?
Answer: A wide-diameter, myelinated axon, such as a motor neuron in a mammal.
Two main factors increase conduction velocity: axon diameter and myelination. A wider diameter reduces the internal resistance to the flow of local currents. Myelination allows for saltatory conduction, where the action potential jumps between nodes of Ranvier. A neuron that has both a wide diameter and is myelinated will have the fastest possible conduction speed. The other options are missing one or both of these features.
- If a single firing from neuron X causes a 10 mV depolarization (an EPSP) and a single firing from neuron Y causes a 10 mV hyperpolarization (an IPSP), what will happen if both neurons X and Y fire simultaneously?
Answer: The two potentials will cancel each other out, and the membrane potential will remain at -70 mV.
This is an example of spatial summation. The EPSP from neuron X (+10 mV) and the IPSP from neuron Y (-10 mV) arrive at the same time. The algebraic sum of these potentials is 0 mV. Therefore, they cancel each other out, and the postsynaptic membrane potential remains at its resting value of -70 mV, so no action potential is fired. The other options represent incorrect calculations of the net potential change.
- If this neuron is then stimulated with a stimulus that would normally be well above the threshold level, what is the most likely outcome?
Answer: The neuron will fail to depolarize, and no action potential will be generated.
Action potentials rely on a rapid influx of Na+ through voltage-gated channels for depolarization. By blocking these channels, TTX prevents this influx. Even with a strong stimulus, the membrane cannot depolarize to initiate an action potential. Choice B is incorrect because action potentials are 'all-or-nothing' events; their amplitude is not graded. Choice C describes the effect of blocking K+ channels. Choice D is incorrect as blocking Na+ influx would prevent depolarization, not cause hyperpolarization.
- What is the direct effect of an SSRI that leads to its therapeutic action?
Answer: It prolongs the presence of serotonin in the synaptic cleft, increasing the likelihood of binding to postsynaptic receptors.
Reuptake is the process by which neurotransmitters are cleared from the synaptic cleft back into the presynaptic neuron. By inhibiting the serotonin transporter, SSRIs block this reuptake. This causes serotonin to remain in the synapse for a longer period, allowing it to repeatedly stimulate the postsynaptic receptors. This enhanced stimulation is believed to be the basis of its therapeutic effect. The other options describe different pharmacological mechanisms.
- Ouabain is a chemical that irreversibly inhibits the sodium-potassium (Na+/K+) pump. If a neuron is treated with ouabain, what is the most likely long-term consequence for its membrane potential and ability to signal?
Answer: The resting membrane potential will gradually move towards 0 mV as ion gradients for Na+ and K+ dissipate, eventually preventing the generation of action potentials.
The Na+/K+ pump is essential for maintaining the steep concentration gradients of Na+ (high outside) and K+ (high inside) across the membrane. Without the pump, these ions will leak down their concentration gradients, causing the gradients to dissipate. As a result, the resting membrane potential, which depends on these gradients, will slowly decay towards zero. Eventually, the gradients will be too weak to support the ion fluxes needed for an action potential. The neuron will become inexcitable.
- A patient suffers an injury that severs the ventral root of a spinal nerve in their lumbar region. Which of the following symptoms would be the most direct result of this specific injury?
Answer: Loss of voluntary muscle control in the corresponding area of the leg, but with retained sensation.
The ventral root of a spinal nerve contains the axons of motor neurons, which carry signals from the spinal cord to the muscles. Severing this root would interrupt motor commands, causing paralysis in the corresponding area. The dorsal root, which carries sensory information, would be unaffected, so sensation would be retained. Choice A describes damage to a dorsal root. Choice B is incorrect because the injury is in the lumbar (leg) region, not the cervical (arm) region. Choice D is incorrect because both reflex and voluntary motor commands would be blocked.
