Questions and Answers
What happens to the membrane potential after Na+ channels inactivate?
What defines the absolute refractory period during an action potential?
What characterizes the delayed activation of K+ channels during an action potential?
What occurs during the relative refractory period of an action potential?
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What is the effect of voltage-gated Na+ channels inactivation on neuronal signaling?
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What happens to the cell during the hyperpolarization phase?
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How does myelination affect nerve signal propagation?
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What is a potential effect of toxins that target ion channels?
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What effect does a toxin that blocks voltage-gated Na+ channels have on action potentials?
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What is the primary trigger for the release of neurotransmitters at the synaptic cleft?
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Which ion's entry into the presynaptic terminal triggers neurotransmitter vesicle fusion?
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How do SNARE proteins contribute to the release of neurotransmitters?
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Which toxin is known to block voltage-gated Na+ channels?
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What physiological effect could result from a toxin altering neurotransmitter release at muscles?
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What happens when voltage-gated Ca+2 channels open in response to an action potential?
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How does myelination affect nerve signal propagation?
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What is the result of a toxin that forces Na+ channels to remain open?
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What role does synaptotagmin play in neurotransmitter release?
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What triggers the opening of voltage-sensitive ion channels?
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What is the threshold voltage required to trigger an action potential?
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What occurs during depolarization of a neuron?
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Which phase follows depolarization in an action potential?
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Which term describes the period during which a neuron cannot generate another action potential?
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How does myelination affect nerve signal propagation?
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What is the primary role of neurotransmitter release at the synaptic cleft?
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What effect do toxins that block ion channels have on action potentials?
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Which statement best describes hyperpolarization during an action potential?
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What initiates the all-or-none response of action potential generation?
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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.
