The Resting Neuron
At rest, a neuron maintains a voltage of about -65mV across its membrane — the inside is negative relative to the outside. This resting potential is maintained by the sodium-potassium pump, which continuously moves 3 Na+ ions out and 2 K+ ions in, and by leak channels that allow some K+ to seep out. This electrochemical gradient is the neuron's stored energy, ready to be released as an action potential. The resting state is not passive — it requires constant energy expenditure, consuming roughly 20% of the brain's total energy budget.
Threshold and the All-or-Nothing Response
When a stimulus depolarizes the membrane to about -55mV (the threshold), a positive feedback loop begins: voltage-gated sodium channels open, Na+ rushes in, depolarizing the membrane further, opening more sodium channels. This explosive cascade drives the voltage to about +40mV in less than a millisecond. Crucially, if the stimulus doesn't reach threshold, nothing happens — the membrane simply returns to rest. And if it does reach threshold, the spike is always the same size. This all-or-nothing property means neurons cannot encode information in spike amplitude; instead, they use firing rate (more spikes per second = stronger signal).
The Hodgkin-Huxley Model
In 1952, Alan Hodgkin and Andrew Huxley published their mathematical model of the action potential in the squid giant axon — work that earned them the 1963 Nobel Prize. Their model describes the membrane as an electrical circuit with variable conductances for sodium and potassium. The sodium conductance depends on three 'activation' gates (m) and one 'inactivation' gate (h); the potassium conductance depends on four activation gates (n). These gates open and close with voltage-dependent rates, producing the characteristic spike shape. Remarkably, this model — developed before the molecular nature of ion channels was known — accurately predicted channel behavior confirmed decades later.
Temperature, Speed, and the Neural Code
Temperature profoundly affects action potential dynamics through the Q10 effect: for each 10°C temperature increase, ion channel kinetics roughly triple in speed. Cold-blooded animals' neurons slow dramatically in winter; warm-blooded animals maintain constant neural processing speed at metabolic cost. The simulation shows how higher temperatures produce faster, narrower spikes with shorter refractory periods, allowing higher firing rates. In myelinated axons, action potentials jump between nodes of Ranvier at up to 120 m/s. This saltatory conduction — combined with the frequency code of spike trains — forms the physical basis of all neural computation.