Action potentials
Page 1: Action Potential and Neuron Physiology
Resting Membrane Potential
Established primarily due to permeability of the membrane to potassium ions (K+).
Initiating Action Potential
Location: Action potential begins at the axon hillock.
Depolarization:
Induced by electrical stimulus.
Involves opening of voltage-gated sodium channels.
Sodium ions (Na+) flow into the cell, shifting membrane potential from negative to positive.
If threshold potential is reached, an action potential is generated.
All-or-Nothing Principle: Action potentials only occur if threshold is met; maximum response if threshold reached.
Returning to Resting State
Voltage-gated Sodium Channels: Close post-depolarization.
Repolarization:
Caused by opening of potassium channels.
K+ ions move out of the cell, making membrane potential more negative, approaching resting potential.
Can overshoot resting potential leading to hyperpolarization.
Na+/K+ ATPase: Not involved in repolarization process.
Refractory Period
Absolute Refractory Period:
Begins after sodium channels close.
Channels become inactive, cannot reopen regardless of membrane potential.
Relative Refractory Period:
Sodium channels recover gradually from inactivation.
Neuron can generate action potential but requires a stronger than normal stimulus.
Initial required stimulus strength is high, decreases as recovery progresses.
Propagation of Action Potentials
Action potentials propagate via local currents.
Local currents induce depolarization in adjacent axon regions, causing new action potentials.
Recently depolarized areas cannot initiate further depolarization due to the refractory period.
Distance of Propagation:
Depends on membrane capacitance and resistance.
Membrane Capacitance: Ability to store charge; lower capacitance allows longer threshold distance.
Page 2: Myelination and Neuronal Signal Transmission
Myelinated Axons
Function: Enhance speed of electrical signal conduction and energy efficiency.
Myelin Sheath:
Forms an insulating layer around axons.
Contains gaps known as Nodes of Ranvier where axonal membrane is exposed.
High density of ion channels at nodes enables action potentials only here.
Improved Conduction: Myelin sheath increases membrane resistance and reduces capacitance.
Saltatory Conduction:
Action potentials jump from node to node, rapidly conducting signals down the neuron.
Action Potentials in the Heart
General Concept: Action potentials trigger contractions in cardiomyocytes through ion fluxes.
Five Phases (0-4) of cardiomyocyte action potential:
Phase 4: Resting Phase
Resting potential of -90 mV due to K+ leaks through inward rectifier channels.
Na+ and Ca2+ channels closed.
Phase 0: Depolarization
Triggered by action potential from a neighboring cell.
Fast Na+ channels open, leading to Na+ influx, raising TMP rapidly toward threshold (-70 mV).
Large Na+ current rapidly depolarizes to 0 mV, causing overshoot.
L-type Ca2+ channels open at TMP > -40 mV.
Phase 1: Early Repolarization
TMP becomes slightly positive.
Some K+ channels open, K+ leaves the cell, returning TMP to around 0 mV.
Phase 2: Plateau Phase
L-type Ca2+ channels remain open, allowing a sustained Ca2+ influx.
K+ outflow occurs, balancing currents to maintain TMP just below 0 mV.
Phase 3: Repolarization
Gradual inactivation of Ca2+ channels.
K+ outflow exceeds Ca2+ inflow, returning TMP to -90 mV.
Ionic gradients restored via Na+-Ca2+ exchanger, Ca2+-ATPase, and Na+-K+-ATPase.