Electrical Signaling in Neurons (4C) - MCAT Chemical and Physical Foundations of Biological Systems

$\text{Na}^+$ has the higher extracellular concentration. Sodium ions are actively pumped out of the neuron by the Na+/K+ ATPase, establishing a higher concentration in the extracellular fluid compared to potassium.

$\text{K}^+$ has the higher intracellular concentration. Potassium ions are actively pumped into the neuron by the Na+/K+ ATPase, resulting in a higher intracellular concentration than sodium.

$E_{Na}$ becomes less positive (moves toward $0$). Decreasing extracellular sodium reduces the concentration gradient, making the equilibrium potential less positive per the Nernst equation.

Negative inside relative to outside (typically about $-70\ \text{mV}$). The resting membrane potential is negative due to the dominance of potassium leak channels and the electrochemical gradients maintained by ion pumps.

$\text{Na}^+/\text{K}^+$ ATPase. The Na+/K+ ATPase actively transports sodium out and potassium in, using ATP to maintain steep ion gradients across the neuronal membrane.

$3\ \text{Na}^+$ out and $2\ \text{K}^+$ in (net $+1$ out). Each cycle hydrolyzes ATP to export three sodium ions and import two potassium ions, contributing to the membrane potential by net positive charge efflux.

$\text{K}^+$ leak channels. Potassium leak channels allow greater passive flux of K+ than other ions at rest, driving the membrane potential close to the potassium equilibrium potential.

The $V_m$ at which net flux of that ion is $0$. The equilibrium potential balances the chemical driving force from concentration gradients with the electrical driving force, resulting in zero net ion movement.

$E=\frac{RT}{zF}\ln\left(\frac{[\text{out}]}{[\text{in}]}\right)$. The Nernst equation calculates the reversal potential based on temperature, valence, and the ratio of extracellular to intracellular ion concentrations.

$E\approx\frac{61\ \text{mV}}{z}\log\left(\frac{[\text{out}]}{[\text{in}]}\right)$. At body temperature, the Nernst equation simplifies to this form for easier computation using base-10 logarithms and millivolt units.

$E_K$ becomes less negative (moves toward $0$). Increasing extracellular potassium reduces the concentration gradient, shifting the equilibrium potential toward zero according to the Nernst equation.

Out of the neuron (down its concentration gradient). At resting potential, the concentration gradient drives potassium efflux, outweighing the opposing electrical gradient.

$V_m$ becomes less negative (moves toward $0$ or positive). Depolarization occurs when positive ion influx or negative ion efflux reduces the magnitude of the negative membrane potential.

$V_m$ becomes more negative than resting potential. Hyperpolarization results from increased potassium efflux or chloride influx, enhancing the negative charge inside the neuron.

Approximately $-55\ \text{mV}$ (cell-type dependent). Threshold is the voltage at which voltage-gated sodium channels open sufficiently to trigger regenerative depolarization in the action potential.

Voltage-gated $\text{Na}^+$ channels. These channels activate at threshold, allowing rapid sodium influx that drives the membrane potential toward the sodium equilibrium potential.

$\text{Na}^+$ channel inactivation plus opening of voltage-gated $\text{K}^+$ channels. Sodium channel inactivation halts influx, while potassium channel opening promotes efflux, restoring the membrane potential to resting levels.

Period when inactivated $\text{Na}^+$ channels cannot reopen. During this period, sodium channels remain in an inactivated state, preventing further action potentials regardless of stimulus strength.

Persistently open $\text{K}^+$ channels and hyperpolarization. Delayed closure of potassium channels causes afterhyperpolarization, raising the threshold for subsequent action potentials.

Regenerative opening of voltage-gated channels along the membrane. Local depolarization triggers sequential activation of voltage-gated channels, regenerating the full amplitude of the action potential at each point along the axon.

Increased myelination. Myelination insulates the axon, reducing capacitance and enabling faster saltatory conduction between nodes of Ranvier.

Nodes of Ranvier. These unmyelinated gaps concentrate voltage-gated channels, allowing regeneration of the action potential and efficient propagation.

Apparent "jumping" of depolarization between nodes in myelinated axons. Myelin prevents ion flux between nodes, allowing passive current spread that depolarizes the next node, speeding conduction.

Resting $V_m$ depolarizes (becomes less negative). Elevated extracellular potassium shifts the potassium equilibrium potential less negative, pulling the resting potential toward it via leak channels.