Questions and Answers
What primarily determines the resting membrane potential in neurons?
What is the threshold membrane potential that triggers an action potential?
Which ion is primarily involved in the rapid depolarization phase of an action potential?
What occurs during the repolarization phase of an action potential?
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Which mechanism allows a neuron's action potential to propagate along the axon?
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What best describes the relative refractory period?
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What is the primary effect of excitatory postsynaptic potentials (EPSPs)?
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Which ion's influx during an action potential leads to neurotransmitter release?
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What defines hyperpolarization in neuronal activity?
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Which statement about ligand-gated ion channels is correct?
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What is the typical range for resting membrane potential in neurons?
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Which ion is pumped out of the cell more than any other by the sodium-potassium ATPase?
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What effect do leaky potassium channels have on resting membrane potential?
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Why does sodium have less impact on resting membrane potential compared to potassium?
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What does the Nernst potential calculate?
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Which of these ions has a higher concentration inside the cell, influencing resting membrane potential?
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What role do unoccupied negative charges inside the cell serve in resting membrane potential?
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What is the primary consequence of the action of sodium-potassium ATPases on ion concentrations?
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What is the approximate Nernst potential for potassium when the concentrations are 5 mM outside and 150 mM inside?
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Which characteristic is NOT true about resting membrane potential?
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Study Notes
Resting Membrane Potential
- Defined as the voltage difference across the cell membrane when a neuron is at rest.
- Exists in all cell types, not just neurons, highlighting its universal biological significance.
- Typical range for resting membrane potential in neurons is between negative 70 to negative 90 millivolts, with negative 70 millivolts being the average.
Mechanisms Contributing to Resting Membrane Potential
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Sodium-Potassium ATPases
- Pumps three sodium ions out of the cell and two potassium ions into the cell.
- Establishes a slight negative charge inside the cell and maintains ion concentration gradients: higher sodium outside and higher potassium inside.
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Leaky Potassium Channels
- Always open, allowing potassium ions to flow in and out of the cell passively.
- Higher potassium concentration inside drives potassium ions to exit, leading to a more negative internal environment.
- Loss of potassium creates unoccupied negative charges (anions) inside, increasing negativity up to around negative 90 millivolts.
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Leaky Sodium Channels
- Also allow sodium ions to flow, but the permeability of the membrane to potassium is much higher than that to sodium.
- Sodium influx contributes less to resting membrane potential adjustment, as much of its concentration remains outside the cell.
Ion Concentration Gradients
- Sodium concentration is higher outside, while potassium concentration is higher inside due to the action of pumps.
- The movement of ions occurs based on their respective concentration gradients, contributing to the overall membrane potential.
Nernst Potential
- Calculated for various ions (e.g., potassium and sodium) to determine their equilibrium potential across the membrane.
- For potassium:
- Equation used: E(K) = 61.5 / z × log([K outside] / [K inside])
- Typical concentrations: 5 mM outside, 150 mM inside yield approximately negative 90 millivolts.
- For sodium:
- Equation: E(Na) = 61.5 / z × log([Na outside] / [Na inside])
- Typical concentrations: 140 mM outside, 10 mM inside yield approximately positive 70 millivolts.
Overall Impact
- The resting membrane potential is determined primarily by the equilibrium potentials of potassium and sodium.
- Significant shifts in membrane potential are primarily due to changes in permeability to potassium, rather than sodium, emphasizing the greater impact of potassium on resting potential stabilization.### Membrane Potentials
- Resting membrane potential is typically around negative 70 millivolts.
- The equilibrium potential for potassium influences the cell voltage when potassium ions move out.
- A cell with 90% permeability to potassium and 10% to sodium would average near negative 70 millivolts.
Graded Potentials
- Graded potentials adjust the resting membrane potential towards the threshold for action potentials.
- Threshold voltage for action potential stimulation is approximately negative 55 millivolts.
- Depolarization moves the membrane potential closer to threshold; hyperpolarization makes it more negative.
- Excitatory postsynaptic potentials (EPSPs) bring the membrane potential closer to threshold.
- Inhibitory postsynaptic potentials (IPSPs) move the potential further from threshold.
Neuronal Communication
- Presynaptic neurons release neurotransmitters (e.g., glutamate for EPSPs, GABA for IPSPs) at the synapse to influence the postsynaptic neuron.
- Ligand-gated ion channels open in response to neurotransmitter binding, allowing ion flow.
- Sodium (Na+) and calcium (Ca2+) influx increases the cell's positive charge.
- Chloride (Cl-) influx or potassium (K+) efflux makes the cell interior more negative, inducing hyperpolarization.
Summation of Potentials
- EPSPs and IPSPs compete to influence membrane potential, with the aim to have more EPSPs to trigger action potentials.
- Temporal summation involves rapid repeated firing from a single presynaptic neuron, cumulatively raising potential.
- Spatial summation involves simultaneous firing from multiple presynaptic neurons, increasing total EPSP effect.
Threshold and Action Potential
- Action potentials are triggered when the threshold of negative 55 millivolts is reached at the axon hillock.
- Voltage-gated sodium channels, concentrated at the axon hillock, open rapidly upon reaching threshold.
- Sodium influx during action potential can elevate membrane potential to positive 30 millivolts, reversing the polarity.
- Once the threshold is reached, voltage-gated channels create an all-or-nothing response, triggering the action potential.### Action Potential and Ion Channels
- Resting Membrane Potential: Neurons have a resting membrane potential around -70 millivolts.
- Threshold Potential: An action potential is initiated when the membrane potential reaches approximately -55 millivolts.
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Voltage-Gated Sodium Channels:
- Activation gate opens at -55 millivolts, allowing sodium (Na+) ions to rush in.
- Positive feedback leads to rapid depolarization, peaking around +30 millivolts.
- Inactivation gate closes at +30 millivolts, preventing further Na+ entry.
Depolarization and Action Potential Propagation
- Depolarization: Movement from a negative to a positive internal charge, specifically when Na+ enters the cell.
- Propagation: The depolarizing wave moves along the axon towards the terminal bulb.
- Voltage-Gated Calcium Channels: Activated at +30 millivolts, allowing calcium (Ca2+) to enter the axon terminal necessary for neurotransmitter release.
Neurotransmitter Release Mechanism
- Synaptic Vesicle Fusion: Calcium binds to SNARE proteins, facilitating the fusion of vesicles with the cell membrane.
- Exocytosis: Release of neurotransmitters into the synaptic space to interact with adjacent neurons.
Repolarization and Hyperpolarization
- Repolarization: Returning the membrane potential back to resting state (-70 millivolts).
- Voltage-Gated Potassium Channels: Open at +30 millivolts, allowing potassium (K+) to exit and move the potential towards -90 millivolts.
- Hyperpolarization: Occurs when the potential goes below -70 millivolts due to excess K+ leaving before returning to resting potential.
Key Definitions
- Depolarization: Making the inside of the cell more positive.
- Repolarization: Returning from a positive back to a negative resting potential.
- Hyperpolarization: Increasing negativity beyond the resting potential.
Recovery to Resting Membrane Potential
- Restoration Mechanisms: Involvement of sodium-potassium ATPase and leak channels help stabilize the membrane potential back to -70 millivolts.
-
Refractory Periods:
- Absolute Refractory Period: Follows peak depolarization where no stimulation can initiate another action potential, regardless of stimulus strength.
- Relative Refractory Period: Occurs after the absolute phase when a stronger-than-normal stimulus is needed to initiate a new action potential.
Summary of Voltage-Gated Channel States
- At Rest: Activation gate closed, inactivation gate open.
- During Depolarization: Activation gate opens, inactivation gate begins to close.
- At Peak Depolarization: Activation gate open, inactivation gate closed.
- During Repolarization: Activation gate begins to close, K+ channels open.
- Post Action Potential: Recovery to resting state configuration upon reaching -70 millivolts.
Resting Membrane Potential
- Voltage difference across the cell membrane in a resting neuron, typically around -70 to -90 millivolts.
- Universal phenomenon observed in all cell types, not just neurons.
Mechanisms Contributing to Resting Membrane Potential
- Sodium-Potassium ATPases: Pumps 3 Na+ ions out and 2 K+ ions in, creating a slight negative interior and maintaining concentration gradients.
- Leaky Potassium Channels: Always open, allowing K+ to exit, enhancing negative charge inside the cell.
- Leaky Sodium Channels: Less impact on resting potential due to lower permeability; primarily sodium remains outside.
Ion Concentration Gradients
- Sodium concentration is higher outside (140 mM) and potassium is higher inside (150 mM).
- Ion movement driven by these gradients influences membrane voltage.
Nernst Potential
- Equilibrium potential calculated to determine ion movement across membranes.
- Potassium: E(K) calculation shows potential around -90 mV based on typical ion concentrations.
- Sodium: E(Na) is approximately +70 mV based on differing concentrations inside and outside.
Overall Impact
- Resting membrane potential highly influenced by potassium equilibrium potential and its permeability.
- Shifts in membrane potential primarily occur due to changes in potassium permeability rather than sodium.
Membrane Potentials
- Average resting membrane potential is about -70 mV.
- Higher potassium permeability results in a more stable resting potential around this value.
Graded Potentials
- Facilitate adjustments to resting potential, moving towards action potential threshold of approximately -55 mV.
- EPSPs bring the potential closer to threshold while IPSPs push it further away.
Neuronal Communication
- Neurotransmitters (e.g., glutamate for EPSPs, GABA for IPSPs) released by presynaptic neurons impact the postsynaptic neuron.
- Ligand-gated ion channels open upon binding of neurotransmitters, allowing ion flow that alters charge inside the neuron.
Summation of Potentials
- EPSPs and IPSPs balance to affect membrane potential; more EPSPs needed to trigger action potentials.
- Temporal summation combines rapid sequential firing from a single neuron.
- Spatial summation accumulates effects from concurrent firings of multiple neurons.
Threshold and Action Potential
- Action potential triggered at -55 mV at axon hillock, where voltage-gated sodium channels open.
- Rapid depolarization occurs as Na+ influx raises potential to +30 mV, reversing polarity.
Action Potential and Ion Channels
- Resting membrane potential around -70 mV; action potential initiation requires reaching the threshold.
- Voltage-gated sodium channels rapidly open at threshold, allowing Na+ entry and causing depolarization.
Depolarization and Action Potential Propagation
- Depolarization occurs when Na+ floods into cells, creating a positive charge.
- Propagation of depolarization signals travels along the axon toward the terminal.
- Voltage-gated calcium channels open at +30 mV, critical for neurotransmitter release.
Neurotransmitter Release Mechanism
- Calcium binds to SNARE proteins aiding vesicle fusion with the membrane for exocytosis of neurotransmitters.
Repolarization and Hyperpolarization
- Repolarization brings the membrane back to about -70 mV.
- Voltage-gated potassium channels open at +30 mV, causing K+ to exit and potential to drop towards -90 mV.
- Hyperpolarization occurs when the potential falls below -70 mV due to excess K+ outflow.
Key Definitions
- Depolarization: Inside of cell becomes more positive.
- Repolarization: Return from a positive back to negative resting potential.
- Hyperpolarization: Increased negativity beyond resting potential.
Recovery to Resting Membrane Potential
- Sodium-potassium ATPase and leak channels help stabilize the membrane back to -70 mV.
-
Refractory Periods:
- Absolute Refractory Period: No further action potentials can be initiated post-depolarization.
- Relative Refractory Period: Follows absolute period; requires a stronger stimulus to generate a new action potential.
Summary of Voltage-Gated Channel States
- At Rest: Activation gates closed, inactivation gate open.
- During Depolarization: Activation gate opens; inactivation gate starts closing.
- At Peak: Both activation gates are open; inactivation gate closes to stop Na+ entry.
- During Repolarization: K+ channels open, returning the cell to a negative state.
- Post Action Potential: Channels recover to resting state configuration as the potential returns to -70 mV.
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Description
This quiz explores the concept of resting membrane potential, focusing on its definition and significance across cell types. Additionally, it examines the mechanisms like sodium-potassium ATPases and leaky potassium channels that contribute to the maintenance of this potential. Test your understanding of these fundamental biological processes.
