Podcast
Questions and Answers
What is the role of the sodium-potassium pump during the falling phase of the action potential (AP)?
What is the role of the sodium-potassium pump during the falling phase of the action potential (AP)?
- It directly controls the opening and closing of the voltage-gated potassium channels.
- It restores the initial concentration gradients of sodium and potassium, preparing the cell for another AP. (correct)
- It directly contributes to the influx of sodium ions (Na+) into the cell.
- It directly contributes to the rapid efflux of potassium ions (K+) out of the cell.
During the falling phase of the AP, why does the potassium channel remain open even after the membrane potential reaches the resting membrane potential (RMP)?
During the falling phase of the AP, why does the potassium channel remain open even after the membrane potential reaches the resting membrane potential (RMP)?
- The potassium channel's closure is delayed due to the slow inactivation kinetics of the potassium channel. (correct)
- The potassium channel is insensitive to changes in membrane potential.
- The potassium channel is directly activated by the influx of sodium ions.
- The potassium channel remains open due to the inactivation of the sodium channel, preventing further sodium influx.
Consider the role of the potassium leak channels during the rising phase of the AP. How does their activity affect the overall action potential?
Consider the role of the potassium leak channels during the rising phase of the AP. How does their activity affect the overall action potential?
- They are primarily responsible for initiating the action potential due to their constant leakiness.
- They contribute to a continuous outward flow of potassium, opposing and slightly slowing the depolarization phase. (correct)
- They play a minor role, as the massive influx of sodium ions overrides their effects.
- They contribute to the rapid inflow of potassium ions, accelerating the depolarization phase.
Which of the following statements correctly describes the inactivation of the sodium channel during the rising phase of the action potential?
Which of the following statements correctly describes the inactivation of the sodium channel during the rising phase of the action potential?
What is the primary consequence of the inactivation of the sodium channels during the falling phase of the action potential?
What is the primary consequence of the inactivation of the sodium channels during the falling phase of the action potential?
What is the role of calcium ions (Ca2+) in neurotransmitter release?
What is the role of calcium ions (Ca2+) in neurotransmitter release?
Which of the following statements accurately describes the difference between electrical and chemical synapses?
Which of the following statements accurately describes the difference between electrical and chemical synapses?
What is the primary function of a neurotransmitter receptor located on the postsynaptic membrane?
What is the primary function of a neurotransmitter receptor located on the postsynaptic membrane?
How does the experimental research described in the text demonstrate the chemical nature of nerve impulse transmission?
How does the experimental research described in the text demonstrate the chemical nature of nerve impulse transmission?
What is the significance of the statement that some neurotransmitters act as "first messengers" and trigger "second messengers"?
What is the significance of the statement that some neurotransmitters act as "first messengers" and trigger "second messengers"?
Which of the following scenarios would directly contribute to a postsynaptic neuron becoming more likely to fire an action potential?
Which of the following scenarios would directly contribute to a postsynaptic neuron becoming more likely to fire an action potential?
What does the concept of "synaptic integration" refer to?
What does the concept of "synaptic integration" refer to?
What is the primary benefit of chemical synapses over electrical synapses, despite the slower transmission speed?
What is the primary benefit of chemical synapses over electrical synapses, despite the slower transmission speed?
How does the neurotransmitter acetylcholine affect cardiac muscle contraction?
How does the neurotransmitter acetylcholine affect cardiac muscle contraction?
Which characteristic distinguishes metabotropic receptors from ionotropic receptors?
Which characteristic distinguishes metabotropic receptors from ionotropic receptors?
How is the release of neurotransmitters from the axon terminal terminated?
How is the release of neurotransmitters from the axon terminal terminated?
Which statement accurately describes the role of calcium ions in neurotransmitter release?
Which statement accurately describes the role of calcium ions in neurotransmitter release?
What is the primary function of the nicotinic acetylcholine receptor?
What is the primary function of the nicotinic acetylcholine receptor?
How does the diversity of neurotransmitter receptors contribute to the complexity of neuronal signaling?
How does the diversity of neurotransmitter receptors contribute to the complexity of neuronal signaling?
What is the main role of enzymes in the process of neurotransmitter removal from the synaptic cleft?
What is the main role of enzymes in the process of neurotransmitter removal from the synaptic cleft?
Why is the binding of acetylcholine to its receptor considered ligand-gated?
Why is the binding of acetylcholine to its receptor considered ligand-gated?
Which of the following statements accurately describes the role of myelin in AP conduction?
Which of the following statements accurately describes the role of myelin in AP conduction?
What is the primary reason why the nodes of Ranvier are crucial for saltatory conduction?
What is the primary reason why the nodes of Ranvier are crucial for saltatory conduction?
Imagine an experimental scenario where the concentration of sodium ions ($Na^+$) is reduced at the nodes of Ranvier. How would this affect saltatory conduction?
Imagine an experimental scenario where the concentration of sodium ions ($Na^+$) is reduced at the nodes of Ranvier. How would this affect saltatory conduction?
How does the structure of the axon hillock in a myelinated neuron compare to that of an unmyelinated neuron?
How does the structure of the axon hillock in a myelinated neuron compare to that of an unmyelinated neuron?
Which of the following best explains why myelinated neurons can achieve significantly higher conduction velocities compared to unmyelinated neurons?
Which of the following best explains why myelinated neurons can achieve significantly higher conduction velocities compared to unmyelinated neurons?
What is the primary difference between the conduction process in myelinated and unmyelinated neurons?
What is the primary difference between the conduction process in myelinated and unmyelinated neurons?
If a toxin preferentially destroyed the myelin sheaths in the peripheral nervous system, what would be the most likely consequence?
If a toxin preferentially destroyed the myelin sheaths in the peripheral nervous system, what would be the most likely consequence?
Which of the following is NOT a characteristic feature of saltatory conduction?
Which of the following is NOT a characteristic feature of saltatory conduction?
Why does the depolarization of the membrane during an action potential trigger the opening of more sodium channels?
Why does the depolarization of the membrane during an action potential trigger the opening of more sodium channels?
Which of the following statements accurately describes the role of the refractory period in the propagation of action potentials?
Which of the following statements accurately describes the role of the refractory period in the propagation of action potentials?
Which of the following factors is NOT a determinant of the speed of action potential conduction in a myelinated axon?
Which of the following factors is NOT a determinant of the speed of action potential conduction in a myelinated axon?
How do dendrites and the cell body differ from the axon in terms of their role in action potential propagation?
How do dendrites and the cell body differ from the axon in terms of their role in action potential propagation?
Why is the action potential conducted unchanged along the axon membrane to the terminals?
Why is the action potential conducted unchanged along the axon membrane to the terminals?
Which of the following statements accurately describes the action potential's behavior in an unmyelinated axon?
Which of the following statements accurately describes the action potential's behavior in an unmyelinated axon?
Which of the following statements correctly compares the speed of action potential conduction in myelinated and unmyelinated axons?
Which of the following statements correctly compares the speed of action potential conduction in myelinated and unmyelinated axons?
Why is the diameter of an unmyelinated axon a significant factor determining the speed of action potential conduction?
Why is the diameter of an unmyelinated axon a significant factor determining the speed of action potential conduction?
Flashcards
Myelinated Axon
Myelinated Axon
An axon surrounded by myelin sheath that increases conduction speed.
Saltatory Conduction
Saltatory Conduction
The process of action potentials jumping between nodes of Ranvier in myelinated axons.
Nodes of Ranvier
Nodes of Ranvier
Small gaps in the myelin sheath where ions can cross the membrane.
Axon Hillock
Axon Hillock
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Electrical Synapse
Electrical Synapse
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Chemical Synapse
Chemical Synapse
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Presynaptic Cell
Presynaptic Cell
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Postsynaptic Cell
Postsynaptic Cell
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Hodgkin-Huxley Cycle
Hodgkin-Huxley Cycle
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Action Potential Propagation
Action Potential Propagation
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Refractory Period
Refractory Period
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Unmyelinated Axon Conduction
Unmyelinated Axon Conduction
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Spike Initiating Zone
Spike Initiating Zone
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Axon Diameter Effect
Axon Diameter Effect
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Ions Flow
Ions Flow
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Sychronous Activity
Sychronous Activity
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Neurotransmitter Release
Neurotransmitter Release
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Ca2+ Influx
Ca2+ Influx
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Postsynaptic Binding
Postsynaptic Binding
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First Messengers
First Messengers
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G-Protein Coupled Receptors
G-Protein Coupled Receptors
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Exocytosis
Exocytosis
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Role of Ca2+ in exocytosis
Role of Ca2+ in exocytosis
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Neurotransmitter removal
Neurotransmitter removal
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Acetylcholine
Acetylcholine
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Ionotropic receptors
Ionotropic receptors
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Nicotinic receptor
Nicotinic receptor
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Metabotropic receptors
Metabotropic receptors
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Muscarinic receptor
Muscarinic receptor
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Depolarization
Depolarization
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Voltage-gated sodium channel (Na+v)
Voltage-gated sodium channel (Na+v)
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Peak depolarization
Peak depolarization
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Repolarization
Repolarization
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Study Notes
Depolarization - Rising Phase of Action Potential (AP)
- Action potentials (APs) rely on ion currents and voltage-gated channels.
- Sodium (Na+) channels are voltage-gated.
- Potassium (K+) channels are voltage-gated.
- Leak channels for Potassium (K+) are always open.
- At time zero (t=0), voltage-gated Na+ and K+ channels are closed.
- Stimulus opens these channels.
- Na+ channels open, causing Na+ ions to flow in.
- The cell becomes more depolarised.
- Na+ channels close and inactivate, the peak of depolarization.
Falling Phase of AP
- Depolarization depends on ion currents and voltage-gated channels.
- Potassium (K+) channels open, causing K+ ions to flow out.
- The cell repolarizes.
- K+ channels remain open briefly beyond the resting membrane potential, causing hyperpolarization.
- The Na+/K+ pump returns the cell to its resting membrane potential.
Hodgkin-Huxley Cycle
- Action potential rise phase involves positive feedback.
- Initial depolarization leads to further membrane depolarization, which increases Na+ flow.
Action Potential Propagation Along Axon
- Action potentials start at the axon hillock.
- They travel along the axon membrane without change.
- Dendrites and cell bodies have K+ channels that prevent backward propagation.
Propagation of Action Potential
- Action potentials move along an axon by the ion flow generated in one segment depolarizing the next.
AP Conduction in Unmyelinated Axons
- Threshold is reduced at the axon hillock (spike-initiating zone).
- Concentration of Na+ channels.
- Current spreads along the membrane toward terminals(new action potential)
AP Conduction in Myelinated Axons
- Myelin sheath insulation prevents ions from crossing the membrane, reducing current loss.
- Ions are concentrated at nodes (nodes of Ranvier) allowing ions to cross the membrane.
- Action potentials "jump" from node to node (saltatory conduction) increasing conduction velocity.
- Axon diameter and myelin sheath affect the speed of conduction.
Synaptic Transmission
- Chemical synapse is where a neuron communicates with another neuron or effector.
- Pre-synaptic neuron releases neurotransmitters into the synaptic cleft.
- Post-synaptic neuron receives the neurotransmitter and responds.
Two Types of Synapses
- Electrical synapses: Direct ion flow between cells. rapid transmission; synchronicity; cannot be modulated, excitatory only.
- Chemical synapses: Neurotransmitter release across a synaptic cleft; slower transmission; can be modulated.
Chemical Synapse
- Pre- and Postsynaptic neurons separated by a synaptic cleft.
- Neurotransmitters stored in vesicles within the axon terminals of the presynaptic neuron.
- Action potential triggers calcium (Ca2+) influx into the axon terminal.
- Neurotransmitter release (exocytosis) into the synaptic cleft.
- Neurotransmitter binds to receptors on the postsynaptic membrane.
- Ion channels open or close, causing postsynaptic response (depolarization or hyperpolarization).
Vesicles Release Neurotransmitter
- Action potentials cause Ca2+ influx through voltage-gated Ca2+ channels.
- Ca2+ causes vesicles to move to the plasma membrane, fuse, and release neurotransmitter into the cleft.
Postsynaptic Binding
- Neurotransmitters bind to postsynaptic receptors.
- Post-synaptic receptors will either be excitatory (depolarization) or inhibitory (hyperpolarization).
- Allows integration of multiple presynaptic inputs.
Neurotransmitters Work in Two Ways
- Some neurotransmitters bind to ligand-gated ion channels in the postsynaptic membrane.
- Others work more slowly via acting as first messengers, binding to G-protein-coupled receptors, triggering a second messenger (leads to opening or closing of gated channels).
Review: Neurotransmitter Release
- Neurotransmitters released from synaptic vesicles in the synaptic cleft by exocytosis.
- Ca2+ ions trigger exocytosis- through voltage-gated Ca2+ channels opened by the arrival of the action potential.
- Neurotransmitter release stops once action potentials cease.
- Neurotransmitters removed from the synaptic cleft by enzymes or taken up by axon terminals or glial cells.
Neurotransmitters
- Diverse kinds and diverse effects.
- Bind to specific receptor proteins on the postsynaptic membrane, causing either stimulation or inhibition of an effector cell (depending on the receptor present).
e.g. Acetylcholine
- Stimulates skeletal muscle, via nicotinic receptors.
- Inhibits cardiac muscle, via muscarinic receptors.
Two Classes of Acetylcholine Receptor Proteins
- Ionotropic receptors: Ligand-gated ion channels. The post-synaptic response is directly dependent on ion current (eg. nicotinic receptor is a Na+ channel).
- Metabotropic receptors: Influencing postsynaptic cells indirectly through a second messenger system (eg. muscarinic receptor).
Experimental Research
- Heart 1 connected to vagus nerve, shows a fast response.
- Heart 2 does not receive signals from the vagus nerve, shows a slower response.
- The solution from heart 1 caused the delayed, but similar response seen in heart 2
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Description
This quiz explores the intricacies of action potentials, focusing on the roles of sodium and potassium channels during various phases. It covers how these channels influence neuronal signaling and neurotransmitter release, along with the differences between electrical and chemical synapses. Test your understanding of these critical neurophysiological concepts!