High-Yield Neuroscience - Neural Transmission & Brain Anatomy

The baseline electrical potential difference across a neuronal membrane at rest, typically $-70\text{ mV}$. It is established primarily by the ${\text{Na}}^{+}/{\text{K}}^{+}$ ATPase pump ($3{\text{ Na}}^{+}$ out, $2{\text{ K}}^{+}$ in) and high resting membrane permeability to ${\text{K}}^{+}$ via leak channels.

Calculates the equilibrium potential ($E_{ion}$) for a single permeable ion across a membrane:

Where $R$ is the universal gas constant, $T$ is temperature in Kelvin, $z$ is ionic valence, $F$ is Faraday's constant, and $[X]$ represents extracellular vs. intracellular ion concentration.

Determines the overall resting membrane potential by factoring in the relative membrane permeabilities ($P$) and concentration gradients of multiple ions simultaneously (${\text{K}}^{+}$, ${\text{Na}}^{+}$, and ${\text{Cl}}^{-}$):

Triggered when membrane potential reaches threshold (approx. $-55\text{ mV}$). Voltage-gated ${\text{Na}}^{+}$ channels open rapidly, causing a massive influx of ${\text{Na}}^{+}$ down its electrochemical gradient, driving the potential toward $+30\text{ mV}$.

At peak voltage (+30 mV), voltage-gated ${\text{Na}}^{+}$ channels inactivate. Voltage-gated ${\text{K}}^{+}$ channels open slowly, leading to ${\text{K}}^{+}$ efflux (repolarization). Delayed closure of ${\text{K}}^{+}$ channels causes transient hyperpolarization (after-hyperpolarization) below $-70\text{ mV}$.

1. Action potential depolarizes axon terminal.
2. Voltage-gated ${\text{Ca}}^{2+}$ channels open, causing rapid ${\text{Ca}}^{2+}$ influx.
3. ${\text{Ca}}^{2+}$ binds synaptotagmin, triggering SNARE complex (synaptobrevin, syntaxin, SNAP-25) assembly.
4. Vesicle fuses with presynaptic membrane, releasing neurotransmitter via exocytosis.

The primary excitatory neurotransmitter in the CNS.