- A certain inhibitory neurotransmitter opens ligand-gated channels that are permeable to chloride ions (Cl-). If the resting membrane potential of the postsynaptic neuron is -65 mV and the equilibrium potential for Cl- is -75 mV, the binding of this neurotransmitter will lead to:
Answer: an influx of Cl-, causing an IPSP.
An ion moves in the direction that will push the membrane potential toward its own equilibrium potential. Here, the membrane is at -65 mV, and the Cl- equilibrium is at -75 mV. To move the potential from -65 mV towards -75 mV (making it more negative), negatively charged Cl- ions must enter the cell. This influx of negative charge makes the neuron more negative (hyperpolarized), which is an inhibitory postsynaptic potential (IPSP).
- The diagram below shows the change in membrane potential during an action potential. A mutation affecting a specific ion channel causes the after-hyperpolarization phase (the 'dip' below resting potential) to be absent, with the membrane potential returning directly to the resting level after repolarization. This mutation most likely affects the properties of which channels?
Answer: Voltage-gated K+ channels, causing them to close immediately as the membrane reaches resting potential.
The after-hyperpolarization phase occurs because the voltage-gated potassium channels, which open to cause repolarization, are slow to close. This allows K+ to continue leaving the cell even after the resting potential is reached, making the membrane temporarily more negative. If this phase is absent, it implies that the K+ channels are closing more quickly, specifically as soon as the resting potential is achieved, preventing the potential from 'overshooting'.
- An action potential propagates unidirectionally from the axon hillock to the axon terminal. The phenomenon most directly responsible for preventing the action potential from traveling backward up the axon is the:
Answer: absolute refractory period, during which sodium channels are inactivated.
As an action potential travels along the axon, the patch of membrane immediately behind the wave of depolarization is in its absolute refractory period. During this period, the voltage-gated sodium channels are in an inactivated state and cannot be reopened, regardless of the stimulus. This effectively prevents the depolarization from spreading backward and ensures the action potential propagates in one direction.
- A postsynaptic neuron has a resting potential of -70 mV and a threshold of excitation of -50 mV. It receives simultaneous input from two presynaptic neurons. Neuron A's input causes a 15 mV hyperpolarizing postsynaptic potential (IPSP). Neuron B's input causes a 30 mV depolarizing postsynaptic potential (EPSP). What is the resulting membrane potential, and will the neuron fire an action potential?
Answer: The membrane potential will be -55 mV, and an action potential will not be fired.
This problem requires multi-step reasoning involving spatial summation. First, calculate the net change in potential: the +30 mV EPSP and the -15 mV IPSP sum to a net depolarization of +15 mV. Second, apply this change to the resting potential: -70 mV + 15 mV = -55 mV. Third, compare the result to the threshold: -55 mV is at the threshold but does not exceed it. Conventionally, the potential must exceed the threshold to fire. Thus, the final potential is -55 mV, and no action potential is generated.
- Chemical synaptic transmission takes about 0.5 ms longer than axon conduction. Why?
Answer: Diffusion across the cleft
At a chemical synapse, neurotransmitter must be released, diffuse across the synaptic cleft, and bind receptors; that diffusion adds the roughly 0.5 ms synaptic delay. Axon conduction is fast, so the error is thinking action potentials are slower. Na+ channel inactivation relates to refractory timing, and transmitter breakdown happens after transmission, not before.
- Myasthenia gravis is an autoimmune disorder that causes muscle weakness. The underlying pathology involves antibodies that bind to and block nicotinic acetylcholine receptors at the neuromuscular junction. This disease is therefore an example of a disruption of:
Answer: postsynaptic signal reception.
The pathology of myasthenia gravis centers on the postsynaptic membrane. The presynaptic neuron correctly synthesizes and releases acetylcholine, and the action potential propagates normally. The problem is that the postsynaptic receptors are blocked or destroyed, impairing the ability of the muscle cell to receive the chemical signal and respond to it, leading to weakness.
- Which statement correctly distinguishes between a graded potential (e.g., an EPSP) and an action potential?
Answer: The amplitude of a graded potential is proportional to the stimulus intensity, whereas an action potential's amplitude is all-or-none.
The defining characteristic that distinguishes graded potentials from action potentials is their amplitude response to stimulus strength. Graded potentials vary in size depending on the strength of the stimulus (e.g., the amount of neurotransmitter released). Action potentials, once the threshold is met, have a fixed, maximum amplitude regardless of the strength of the triggering stimulus. The other options reverse the properties of the two potential types.
- In a demyelinating disease such as multiple sclerosis, the myelin sheath surrounding axons degenerates. This degradation impairs neuronal communication primarily because it...
Answer: allows the passive electrical current between nodes of Ranvier to decay below the threshold of the next node.
Myelin acts as an electrical insulator, preventing ion leakage across the axonal membrane. This allows the electrical current generated by an action potential at one node of Ranvier to travel quickly and with minimal decay (decrement) to the next node. Without myelin, this current dissipates and weakens significantly over distance, often failing to depolarize the next node to its threshold potential, thus halting the propagation of the signal.
- The 'decision' for a neuron to fire an action potential is made at the axon hillock, where graded potentials are integrated. The axon hillock serves as this integration point because its membrane has a significantly higher density of which component compared to the dendrites or soma?
Answer: Voltage-gated sodium channels
The axon hillock (and the adjacent initial segment of the axon) is the spike initiation zone. Its special status comes from having a much higher concentration of voltage-gated sodium channels than the cell body or dendrites. This high density lowers the threshold for generating an action potential in this region, making it the point where the sum of all incoming EPSPs and IPSPs is most likely to trigger a full, all-or-none action potential.
- During the repolarization phase of an action potential, the permeability of the axonal membrane to which ion increases dramatically?
Answer: K+, as it flows out of the cell
Repolarization is the process of returning the membrane potential to its negative resting state after the peak of depolarization. This is achieved by the opening of voltage-gated potassium (K+) channels. Because the concentration of K+ is much higher inside the cell than outside, opening these channels causes a rapid efflux (outflow) of positively charged K+ ions, making the inside of the cell more negative and driving the potential back towards rest.
- Botulinum toxin (Botox) induces muscle paralysis by preventing the release of acetylcholine at the neuromuscular junction. It accomplishes this by cleaving SNARE proteins. This mechanism of action indicates that the toxin directly interferes with:
Answer: the process of vesicle fusion with the presynaptic membrane.
When you encounter questions about neurotransmitter release, focus on the step-by-step process of synaptic transmission. Understanding where specific proteins and toxins act in this cascade is crucial for psychology students studying neural communication.
Botulinum toxin's mechanism reveals exactly how neurotransmitter release works at the molecular level. SNARE proteins are essential for the final step of neurotransmitter release—they literally pull synaptic vesicles to the presynaptic membrane and allow them to fuse, dumping their contents into the synaptic cleft. When Botox cleaves these proteins, it's like cutting the ropes that would normally dock and open the vesicles. The acetylcholine is still there, still synthesized normally, but it remains trapped inside the vesicles and can't be released.
Option A correctly identifies this vesicle fusion interference. Option B is wrong because the toxin acts presynaptically—it prevents acetylcholine from even reaching the postsynaptic receptors, so receptor binding isn't the direct target. Option C misses the mark because acetylcholine synthesis continues normally; the problem is release, not production. Option D is incorrect because action potentials still propagate down the axon just fine—the breakdown occurs specifically at the release machinery in the terminal.
For psychology exams, remember that neurotoxins typically target specific steps in synaptic transmission. Always trace through the sequence: action potential → calcium influx → vesicle fusion → neurotransmitter release → receptor binding. Identifying which step is disrupted will guide you to the correct answer.
- Temporal summation differs from spatial summation in that temporal summation involves:
Answer: the summing of postsynaptic potentials generated at the same synapse in rapid succession.
Temporal summation occurs when a single presynaptic neuron fires repeatedly and rapidly, causing postsynaptic potentials (PSPs) to be generated before the previous ones have fully decayed. These successive PSPs add together, or summate, over time. In contrast, spatial summation involves the integration of PSPs generated simultaneously at different synapses on the postsynaptic neuron.
- A drug is administered that acts as an antagonist at a specific type of postsynaptic receptor. This means the drug will:
Answer: bind to the receptor without activating it, thereby blocking the neurotransmitter from binding.
By definition, a receptor antagonist is a substance that binds to a receptor but does not elicit the biological response that the natural ligand (agonist) would. In doing so, it occupies the binding site and physically prevents the natural neurotransmitter from binding and activating the receptor, effectively blocking the signal. This is in contrast to an agonist, which would mimic the neurotransmitter's effect.
- A novel neurotoxin is discovered that selectively and permanently binds to voltage-gated sodium channels, locking them in their inactivated state. If a neuron is exposed to this toxin after it has just fired a single action potential, what will be the long-term consequence for this neuron's ability to communicate?
Answer: The neuron will be permanently unable to generate another action potential at the axon hillock.
The ability to generate an action potential depends on the ability of voltage-gated sodium channels to open from a closed state. The inactivated state is a temporary state during the refractory period from which channels must recover before they can open again. If the toxin locks them in this inactivated state, they can never be opened, and thus no action potential can be generated. This is distinct from simply blocking the channels; it traps them in a post-firing state.
- A researcher uses a drug that specifically prevents the action of the enzyme acetylcholinesterase at the neuromuscular junction. What is the most likely immediate effect on the postsynaptic muscle cell when the presynaptic neuron fires?
Answer: The muscle cell will experience a prolonged period of depolarization and contraction.
Acetylcholinesterase is the enzyme responsible for breaking down acetylcholine in the synaptic cleft, terminating its signal. Inhibiting this enzyme means that acetylcholine will not be cleared from the synapse efficiently. It will continue to bind to postsynaptic receptors, causing prolonged depolarization of the muscle cell and, consequently, a sustained or spastic contraction.
- A neuron's relative refractory period is characterized by the fact that:
Answer: a stronger-than-normal stimulus is required to trigger another action potential.
Understanding neuronal excitability requires knowing the different phases of the action potential cycle. After a neuron fires, it goes through two recovery periods that affect its ability to fire again.
During the relative refractory period, the neuron is hyperpolarized (more negative than resting potential) due to continued potassium efflux and active sodium-potassium pump activity. While the voltage-gated sodium channels have recovered from inactivation and can open again, the membrane potential is further from threshold than normal. This means you need a stronger stimulus to reach the threshold voltage and trigger another action potential. This is exactly what answer D describes.
Let's examine why the other options are incorrect. Answer A describes the absolute refractory period, not the relative refractory period. During the absolute refractory period, sodium channels are completely inactivated and no stimulus can trigger firing. Answer B is also describing the absolute refractory period, when sodium channels are stuck in their inactivated state. Answer C, while the sodium-potassium pump is indeed active during recovery, this isn't the defining characteristic of the relative refractory period—the pump works continuously, not just at maximum rate during this phase.
When studying action potentials, create a clear mental timeline: resting → depolarization → repolarization → absolute refractory (impossible to fire) → relative refractory (harder to fire) → return to resting. Remember that "relative" means firing is relatively more difficult, not impossible, distinguishing it from the absolute refractory period.
- After an action potential peaks at +30 mV, what directly restores the resting potential?
Answer: Na+ inactivates and K+ exits
At the peak of the action potential, voltage-gated Na+ channels inactivate, stopping Na+ entry, while voltage-gated K+ channels open and K+ flows out. This loss of positive charge makes the membrane potential return to rest. The tempting wrong idea is that Na+ exits and K+ enters, but Na+ enters during depolarization and K+ exits during repolarization.
- If the sodium-potassium (Na+/K+) pump in a neuron were deactivated by a poison, which of the following would be the most accurate description of the immediate and subsequent effects?
Answer: The neuron could still fire many action potentials, but the Na+ and K+ concentration gradients would slowly diminish over time.
The Na+/K+ pump's primary role is to maintain the long-term concentration gradients of Na+ and K+. It is not directly involved in the rapid depolarization or repolarization phases of a single action potential. A single action potential uses only a tiny fraction of the ions available. Therefore, if the pump stops, the neuron can continue to fire for some time using the existing gradients. However, over time, these gradients would dissipate due to ion leakage and the cumulative effect of many action potentials, eventually rendering the neuron unable to fire.
- The direct trigger for the fusion of synaptic vesicles with the presynaptic membrane and the subsequent release of neurotransmitters is the influx of which ion into the axon terminal?
Answer: Calcium (Ca2+)
While the action potential itself is propagated by the movement of Na+ and K+ ions, the critical step that links the arrival of the action potential at the axon terminal to neurotransmitter release is the opening of voltage-gated calcium channels. The resulting influx of Ca2+ into the terminal acts as an intracellular signal that initiates the cascade of events leading to vesicle fusion and exocytosis of neurotransmitters.
- A brief electrical stimulus triggers an action potential at the midpoint of a resting axon. What occurs?
Answer: APs travel in both directions
A suprathreshold electrical stimulus at the midpoint depolarizes the membrane past threshold, so an action potential is generated at that spot and spreads to adjacent regions on both sides. Since the axon is uniform and has no one-way gate at the stimulus site, the impulse is not restricted to the terminal direction. The tempting error is assuming action potentials always move only toward the terminal, but that is only true when they start at the soma end.
