Etterhyperpolarisering

Etterhyperpolarisering, or etterhyperpolarisering in Norwegian, is the transient hyperpolarization of a neuron’s membrane potential that follows an action potential. After the spike, the membrane potential briefly becomes more negative than the resting level, typically due to potassium efflux and other currents that outlast the repolarization phase. This event reduces the likelihood of immediate subsequent firing and helps shape the neuron's response to input.

There are three main components of afterhyperpolarization: fast AHP (fAHP), medium AHP (mAHP), and slow AHP (sAHP). The fast component lasts roughly 1–5 ms and contributes to rapid repolarization of the spike and the refractory period. The medium component lasts tens to hundreds of milliseconds and is a major determinant of spike-frequency adaptation. The slow component can extend for hundreds of milliseconds up to seconds in some neurons and varies considerably across cell types.

Mechanistically, the fAHP is largely due to activation of voltage-gated and calcium-activated potassium channels that rapidly carry K+ out of the cell. The mAHP is predominantly mediated by small-conductance calcium-activated potassium channels (SK channels) opened by Ca2+ influx during the action potential. The sAHP is less well understood and may involve a combination of calcium-activated processes, different potassium channels, and in some cells the activity of the Na+/K+ ATPase.

Functionally, AHP shapes neuronal excitability by modulating inter-spike intervals and firing patterns. It contributes to spike-frequency adaptation, influences rhythmic activity, and helps prevent excessive firing in response to sustained input. Pharmacological tools such as apamin (SK blocker) and iberiotoxin (BK channel blocker) are used to study the distinct contributions of AHP components.