Action Potentials and Synaptic Transmission (3A) - MCAT Biological and Biochemical Foundations of Living Systems

A receptor that directly opens an ion channel upon binding. Neurotransmitter binding induces a conformational change that directly gates ion flow, producing rapid postsynaptic responses.

$\text{Ca}^{2+}$ influx through voltage-gated $\text{Ca}^{2+}$ channels. Arrival of an action potential depolarizes the terminal, opening these channels and allowing calcium entry to trigger vesicle fusion and exocytosis.

$\text{K}^+$. High intracellular potassium concentration establishes a gradient that, when channels open, allows efflux, restoring the membrane potential to resting levels.

$\text{Na}^+$. High extracellular sodium concentration creates a gradient that, upon channel opening, drives influx, causing rapid depolarization during action potentials.

Approximately $-55\ \text{mV}$. At this potential, voltage-gated sodium channels begin to open, leading to rapid depolarization if the stimulus is sufficient to initiate an action potential.

Summation of repeated inputs over time at one synapse. Repeated subthreshold stimuli from the same presynaptic neuron accumulate, potentially reaching threshold if occurring within a short time frame.

Acetylcholine. Acetylcholinesterase rapidly hydrolyzes acetylcholine into choline and acetate, terminating its signaling at cholinergic synapses.

Reuptake, enzymatic degradation, and diffusion away. These processes clear neurotransmitters from the cleft, preventing prolonged receptor activation and allowing synapse reset.

Summation of inputs from multiple synapses at once. Simultaneous subthreshold inputs from different presynaptic neurons integrate at the postsynaptic cell, possibly summating to threshold.

Stronger stimulus needed; membrane is hyperpolarized. Hyperpolarization during this period raises the threshold, requiring a larger depolarizing stimulus to initiate another action potential.

Sites of high voltage-gated channel density for regeneration. These unmyelinated gaps concentrate voltage-gated sodium channels, allowing action potential regeneration and saltatory conduction.

Refractory period behind the depolarization wave. The absolute refractory period ensures unidirectional propagation by preventing re-excitation in recently depolarized segments.

Once threshold is reached, amplitude is constant. Action potentials are regenerative events where, once initiated, voltage-gated channels ensure a fixed amplitude and duration independent of stimulus intensity.

Myelination. Myelin sheath insulates the axon, promoting saltatory conduction and reducing capacitance for quicker signal propagation.

No new action potential; $\text{Na}^+$ channels are inactivated. During this phase, sodium channels remain inactivated, preventing depolarization regardless of stimulus strength until they reset.

Delayed closing of voltage-gated $\text{K}^+$ channels. Continued potassium efflux after sodium channels close hyperpolarizes the membrane below resting potential before returning to baseline.

Voltage-gated $\text{K}^+$ channels open; $\text{K}^+$ efflux. At peak depolarization, sodium channels inactivate while potassium channels open, permitting potassium outflow that repolarizes the membrane.

Voltage-gated $\text{Na}^+$ channels open; $\text{Na}^+$ influx. Depolarization to threshold activates these channels, allowing rapid sodium entry that further depolarizes the membrane in a positive feedback loop.

Maintains $\text{Na}^+$ out and $\text{K}^+$ in using ATP. The pump actively transports three sodium ions out and two potassium ions in per ATP molecule, establishing ion gradients essential for resting potential and action potentials.

Increased axon diameter. Larger diameter reduces internal resistance to current flow, enabling faster passive spread of depolarization along the axon.