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Questions and Answers
What happens to the membrane potential after Na+ channels inactivate?
What happens to the membrane potential after Na+ channels inactivate?
- The membrane potential decreases. (correct)
- The membrane becomes hyperpolarized.
- The membrane potential becomes unstable.
- The membrane remains depolarized indefinitely.
What defines the absolute refractory period during an action potential?
What defines the absolute refractory period during an action potential?
- Na+ channels are inactivated and cannot open again. (correct)
- The cell is hyperpolarized and inactive.
- The K+ channels have fully opened.
- Both Na+ and K+ channels are closed.
What characterizes the delayed activation of K+ channels during an action potential?
What characterizes the delayed activation of K+ channels during an action potential?
- They open immediately upon depolarization.
- They activate slowly and allow K+ to flow out. (correct)
- They cause immediate depolarization of the membrane.
- They remain closed regardless of membrane potential.
What occurs during the relative refractory period of an action potential?
What occurs during the relative refractory period of an action potential?
What is the effect of voltage-gated Na+ channels inactivation on neuronal signaling?
What is the effect of voltage-gated Na+ channels inactivation on neuronal signaling?
What happens to the cell during the hyperpolarization phase?
What happens to the cell during the hyperpolarization phase?
How does myelination affect nerve signal propagation?
How does myelination affect nerve signal propagation?
What is a potential effect of toxins that target ion channels?
What is a potential effect of toxins that target ion channels?
What effect does a toxin that blocks voltage-gated Na+ channels have on action potentials?
What effect does a toxin that blocks voltage-gated Na+ channels have on action potentials?
What is the primary trigger for the release of neurotransmitters at the synaptic cleft?
What is the primary trigger for the release of neurotransmitters at the synaptic cleft?
Which ion's entry into the presynaptic terminal triggers neurotransmitter vesicle fusion?
Which ion's entry into the presynaptic terminal triggers neurotransmitter vesicle fusion?
How do SNARE proteins contribute to the release of neurotransmitters?
How do SNARE proteins contribute to the release of neurotransmitters?
Which toxin is known to block voltage-gated Na+ channels?
Which toxin is known to block voltage-gated Na+ channels?
What physiological effect could result from a toxin altering neurotransmitter release at muscles?
What physiological effect could result from a toxin altering neurotransmitter release at muscles?
What happens when voltage-gated Ca+2 channels open in response to an action potential?
What happens when voltage-gated Ca+2 channels open in response to an action potential?
How does myelination affect nerve signal propagation?
How does myelination affect nerve signal propagation?
What is the result of a toxin that forces Na+ channels to remain open?
What is the result of a toxin that forces Na+ channels to remain open?
What role does synaptotagmin play in neurotransmitter release?
What role does synaptotagmin play in neurotransmitter release?
What triggers the opening of voltage-sensitive ion channels?
What triggers the opening of voltage-sensitive ion channels?
What is the threshold voltage required to trigger an action potential?
What is the threshold voltage required to trigger an action potential?
What occurs during depolarization of a neuron?
What occurs during depolarization of a neuron?
Which phase follows depolarization in an action potential?
Which phase follows depolarization in an action potential?
Which term describes the period during which a neuron cannot generate another action potential?
Which term describes the period during which a neuron cannot generate another action potential?
How does myelination affect nerve signal propagation?
How does myelination affect nerve signal propagation?
What is the primary role of neurotransmitter release at the synaptic cleft?
What is the primary role of neurotransmitter release at the synaptic cleft?
What effect do toxins that block ion channels have on action potentials?
What effect do toxins that block ion channels have on action potentials?
Which statement best describes hyperpolarization during an action potential?
Which statement best describes hyperpolarization during an action potential?
What initiates the all-or-none response of action potential generation?
What initiates the all-or-none response of action potential generation?
Study Notes
Action Potential and Toxins
- Exposure to toxins that block voltage-gated Na+ channels results in the inability to generate action potentials.
- Toxins like tetrodotoxin (from puffer fish) and saxitoxin (from algae) inhibit Na+ channel function.
- Batrachotoxin (from frogs) causes Na+ channels to remain open, disrupting normal action potential generation.
- Agitoxin (from scorpions) and beta-bungarotoxin (from snakes) target and block voltage-gated K+ channels.
Neurotransmitter Release Mechanism
- An action potential at the presynaptic axon terminal opens voltage-gated Ca²⁺ channels.
- Calcium ions (Ca²⁺) influx is crucial for neurotransmitter release.
- Ca²⁺ promotes the fusion of synaptic vesicles with the presynaptic membrane, leading to exocytosis of neurotransmitters.
Exocytosis Steps
- Neurotransmitter vesicles dock at the axon terminal using SNARE proteins (v-SNARES and t-SNARES).
- Upon action potential arrival, Ca²⁺ binds to synaptotagmin, facilitating vesicle fusion with the axon membrane.
- This results in neurotransmitter release into the synaptic cleft.
Voltage-Gated Channel Dynamics
- After ~1 millisecond, voltage-gated Na+ channels inactivate, marking the absolute refractory period during which additional action potentials cannot occur.
- This inactivation prevents Na+ from re-entering the cell until the channels are reactivated.
K+ Channel Action
- During action potential repolarization, voltage-gated K+ channels open slowly, allowing K+ to exit the cell.
- This results in membrane hyperpolarization, contributing to the relative refractory period where a stronger stimulus is needed to generate another action potential.
Action Potential Phases
- A stimulus causes initial small depolarization of the neuron to the threshold (approximately -40 to -55 mV), triggering an action potential if the axon hillock approves.
- Phase transitions include:
- Depolarization: Cell interior becomes positive.
- Repolarization: Membrane potential returns to a negative value.
- Hyperpolarization: Membrane potential dips below resting membrane potential (RMP), entering the refractory period before returning to RMP.
Membrane Potential Changes
- Various ions affect membrane potential:
- Influx of cations (e.g., Na⁺) leads to depolarization.
- Efflux of cations or influx of anions can cause hyperpolarization, making the neuron more negative.
- Action potentials follow an all-or-nothing principle; once threshold is reached, they occur fully.
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Description
This quiz focuses on the effects of toxins that block voltage-gated Na+ channels on action potentials. It includes a class question regarding the consequences of such exposure. Understand how these toxins impact neural signaling and learn about the mechanisms involved.
