- During the repolarization phase of an action potential, what is the status of the principal voltage-gated ion channels?
Answer: Voltage-gated Na⁺ channels are inactivated, and voltage-gated K⁺ channels are open.
Repolarization is caused by the efflux of K⁺ ions. This occurs because the voltage-gated K⁺ channels are open. At the same time, the voltage-gated Na⁺ channels are in an inactivated state, which prevents Na⁺ influx and also contributes to the absolute refractory period.
- A motor neuron has its cell body located in the spinal cord and its axon terminating on a muscle in the arm. The cell body is part of the _____, while the axon is part of the _____.
Answer: central nervous system (CNS); peripheral nervous system (PNS)
The central nervous system (CNS) consists of the brain and spinal cord. The peripheral nervous system (PNS) consists of all nerves that extend outside the CNS. The cell body (soma) of a motor neuron is located within the grey matter of the spinal cord (CNS), while its axon extends outwards to connect with muscles, making the axon part of the PNS.
- A neuron has a resting potential of -70 mV and a threshold potential of -50 mV. It receives two simultaneous excitatory signals (EPSPs) of +15 mV each and one inhibitory signal (IPSP) of -10 mV. What will be the resulting membrane potential at the axon hillock and will an action potential be generated?
Answer: The potential will be -50 mV, and an action potential will be generated.
The net change in potential is calculated by summing the inputs: (+15 mV) + (+15 mV) + (-10 mV) = +20 mV. The new membrane potential will be the resting potential plus this change: -70 mV + 20 mV = -50 mV. Since this potential reaches the threshold of -50 mV, an action potential will be generated.
- A drug that functions as a selective serotonin reuptake inhibitor (SSRI) is administered. How does this drug affect signalling at a serotonergic synapse?
Answer: It increases the concentration and duration of serotonin in the synaptic cleft.
Reuptake inhibitors work by blocking the transporter proteins on the presynaptic membrane that normally remove the neurotransmitter from the synaptic cleft. By inhibiting this process, the drug causes serotonin to remain in the cleft for a longer period, increasing its concentration and enhancing its effect on the postsynaptic neuron.
- What is the defining characteristic of the threshold potential?
Answer: The membrane potential at which the opening of voltage-gated Na⁺ channels becomes a regenerative, positive feedback loop.
The threshold potential is the critical level of depolarization that must be reached to trigger an action potential. At this potential, the influx of Na⁺ through opening voltage-gated Na⁺ channels overcomes the outward leak of K⁺. This causes further depolarization, which opens more Na⁺ channels, creating a positive feedback cycle that leads to the rapid spike of the action potential.
- Which of the following represents a key difference between a graded potential (like an EPSP) and an action potential?
Answer: The amplitude of a graded potential varies with stimulus strength, while an action potential is all-or-none.
A fundamental distinction is that graded potentials (EPSPs and IPSPs) vary in size depending on the amount of neurotransmitter released. In contrast, an action potential has a fixed amplitude; as long as the threshold is reached, it will fire with the same peak voltage. The other options mischaracterize the properties: graded potentials decay locally (C) and are generated by ligand-gated channels (D), while action potentials are all-or-none depolarizations (A).
- A neurotoxin is discovered that specifically blocks voltage-gated calcium channels at the presynaptic terminals of motor neurons. What is the most immediate consequence of this toxin at the neuromuscular junction?
Answer: Neurotransmitter vesicles will not fuse with the presynaptic membrane.
The influx of Ca²⁺ through voltage-gated calcium channels at the presynaptic terminal is the direct trigger for the fusion of synaptic vesicles with the membrane and the subsequent release of neurotransmitters. Blocking these channels would prevent this fusion. The action potential propagation itself (A) depends on Na⁺ and K⁺ channels. Postsynaptic repolarization (B) and acetylcholinesterase activity (D) are events that occur after neurotransmitter release and binding.
- How does a sensory neuron encode and transmit information about the intensity of a stimulus, such as the difference between a light touch and a firm press?
Answer: By increasing the frequency of action potentials fired per unit of time.
Action potentials operate on an 'all-or-none' principle, meaning their amplitude is constant. The speed of conduction is also constant for a given axon. The nervous system encodes stimulus intensity by modulating the frequency of action potentials. A more intense stimulus generates a higher frequency of firing.
- A neuron is treated with a drug that inhibits the sodium-potassium pump. What is the expected long-term effect on the neuron's resting potential and ability to fire action potentials?
Answer: The resting potential will gradually become less negative, eventually preventing the generation of action potentials.
The sodium-potassium pump actively transports 3 Na⁺ out and 2 K⁺ in, maintaining the concentration gradients essential for the negative resting potential. Inhibiting the pump allows these gradients to slowly dissipate through leak channels, causing the resting potential to become less negative (depolarize). Eventually, the gradients will be too weak to support the generation of an action potential.
- What is the primary advantage of saltatory conduction in myelinated axons compared to continuous conduction in unmyelinated axons?
Answer: It allows for a much faster propagation of the action potential with less energy expenditure.
Saltatory conduction, where the action potential 'jumps' between nodes of Ranvier, is significantly faster than continuous propagation. It is also more energy-efficient because the Na⁺/K⁺ pumps only need to restore ion gradients at the nodes, not along the entire length of the axon membrane.
- A simple reflex arc, such as withdrawing a hand from a hot object, involves a sensory neuron, a relay neuron (interneuron), and a motor neuron. What is the role of the relay neuron in this circuit?
Answer: To form a synapse with the sensory neuron and the motor neuron within the CNS.
In a polysynaptic reflex arc, the relay neuron (or interneuron) is located entirely within the central nervous system (CNS). It serves as a connection point, receiving a signal from the sensory neuron and transmitting it to the motor neuron, allowing for processing within the spinal cord.
- [HL only] Neonicotinoid pesticides act as agonists at nicotinic acetylcholine receptors in insects. This means they bind to and activate the receptors, but are not broken down by acetylcholinesterase. What is the ultimate effect on the insect's nervous system?
Answer: Continuous, uncontrolled stimulation of postsynaptic neurons, leading to spastic paralysis.
By constantly activating the acetylcholine receptors, neonicotinoids cause continuous firing of the postsynaptic neurons. This overstimulation leads to uncontrolled muscle contractions (spastic paralysis), exhaustion, and eventual death of the insect. The effect is persistent because the pesticide is not removed from the receptor or the synapse.
- A postsynaptic neuron receives input from an inhibitory synapse. The neurotransmitter released binds to receptors that open ligand-gated Cl⁻ channels. If the neuron's resting potential is -65 mV and the equilibrium potential for Cl⁻ is -70 mV, what will be the effect?
Answer: A small hyperpolarization known as an Inhibitory Postsynaptic Potential (IPSP).
Opening Cl⁻ channels will cause Cl⁻ ions to flow down their electrochemical gradient. Since the membrane potential (-65 mV) is less negative than the Cl⁻ equilibrium potential (-70 mV), Cl⁻ ions will flow into the cell, making the inside more negative. This small hyperpolarization is an IPSP, which makes it harder for the neuron to reach its firing threshold.
- Local anaesthetics, like lidocaine, block pain by binding to voltage-gated sodium channels. Which part of the neural signalling process is directly inhibited?
Answer: The generation of the depolarization phase of the action potential.
The rapid depolarization phase of an action potential is caused by a massive influx of Na⁺ ions through voltage-gated sodium channels. By blocking these channels, local anaesthetics prevent the neuron from reaching the threshold and firing an action potential. Without an action potential, the pain signal cannot be transmitted to the CNS.
- [HL only] What would be the consequence for an action potential if a drug were to block the inactivation gate of voltage-gated Na⁺ channels, leaving them able to open and close but not inactivate?
Answer: The repolarization phase of the action potential would be significantly prolonged.
The inactivation of Na⁺ channels is crucial for shutting off the influx of Na⁺ and allowing the K⁺ efflux to repolarize the membrane. If the channels could not inactivate, they would remain open as long as the membrane was depolarized, counteracting the repolarizing effect of K⁺ efflux. This would lead to a much-prolonged action potential and a delayed return to the resting state.
- Which statement accurately describes the state of ion gradients and membrane permeability in a neuron at resting potential?
Answer: The concentration of K⁺ is higher inside the cell, and the membrane is most permeable to K⁺.
At rest, the Na⁺/K⁺ pump establishes high K⁺ concentration inside the cell and high Na⁺ concentration outside. The resting membrane's permeability is primarily determined by potassium 'leak' channels, which are open. Therefore, the membrane is much more permeable to K⁺ than to Na⁺, and the outward leak of positive K⁺ ions is the main reason for the negative resting potential.
- What is the direct role of the myelin sheath in nerve impulse transmission?
Answer: It acts as an electrical insulator, forcing the action potential to regenerate only at the nodes of Ranvier.
The myelin sheath is a lipid-rich layer that provides electrical insulation. It prevents the leakage of ions across the axon membrane in the internodal regions. This forces the ionic current to flow down the axon to the next node of Ranvier, where the high concentration of voltage-gated channels allows the action potential to be regenerated. This process is called saltatory conduction.
- The absolute refractory period after an action potential is a brief time when a second action potential cannot be initiated, regardless of stimulus strength. What is the molecular basis for this period?
Answer: The inactivation of voltage-gated Na⁺ channels.
The absolute refractory period is caused by the inactivation gates of the voltage-gated Na⁺ channels closing. Until these gates reset to their resting state, they cannot be opened by depolarization, making a new action potential impossible. The slow closing of K⁺ channels (A) contributes to the relative refractory period.
- After an action potential, the membrane briefly hyperpolarizes, becoming more negative than the resting potential. Which event is the primary cause of this hyperpolarization?
Answer: The voltage-gated K⁺ channels remaining open after the membrane has repolarized.
Voltage-gated potassium channels are slower to close than voltage-gated sodium channels. After the membrane potential returns to the resting level during repolarization, some K⁺ channels are still open, allowing K⁺ to continue leaving the cell. This extra efflux of positive charge makes the membrane temporarily more negative than the normal resting potential.
- Nerve impulses travel in one direction along an axon, from the axon hillock to the terminal. What is the primary reason for this unidirectional propagation?
Answer: The refractory period following an action potential prevents backward propagation.
When a segment of the axon membrane fires an action potential, it enters a refractory period during which its voltage-gated Na⁺ channels are inactivated. This prevents the action potential from re-stimulating the segment it just passed. Therefore, the wave of depolarization can only move forward, away from the region that is currently refractory.
