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Axon hillock: Wikis


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"Hillock" redirects here. A hillock is also a small hill.
The arrow labeled "axon" is pointing directly at the axon hillock.

The axon hillock is the anatomical part of a neuron that connects the cell body (the soma) to the axon. It is the location where the summation of inhibitory postsynaptic potentials (IPSPs) and excitatory postsynaptic potentials (EPSPs) from numerous synaptic inputs on the dendrites or cell body occurs.

It is electrophysiologically equivalent to the initial segment where the summated membrane potential reaches the triggering threshold, an action potential propagates through the rest of the axon (and "backwards" towards the dendrites as seen in neural backpropagation). The triggering is due to positive feedback between highly crowded voltage gated sodium channels, which are present at the critical density at the axon hillock (and nodes of ranvier) but not in the soma.

The axon hillock also functions as a tight junction, since it acts as a barrier for lateral diffusion of transmembrane proteins, GPI anchored proteins such as thy1, and lipids embedded in the plasma membrane.

The positive point, at which the action potential starts, varies between cells. It can also be altered by hormonal stimulation of the neuron, or by second messenger effects of neurotransmitters.


In its resting state, a neuron is polarized, with its inside at about -60mV relative to its surroundings. When an excitatory neurotransmitter is released by the presynaptic neuron bind to the postsynaptic dendritic spines, Ligand-gated ion channel open, allowing sodium ions to enter the cell. This may make the postsynaptic membrane depolarized (less negative). This depolarization will travel towards the axon hillock, diminishing exponentially with time and distance. If several such events occur in a short time, the axon hillock may become sufficiently depolarized for the voltage gated sodium channels to open. This initiates an action potential that then propagates down the axon.

As sodium enters the cell, the cell membrane potential becomes more positive, which activates even more sodium channels in the membrane. The sodium influx eventually overtakes the potassium efflux (via the potassium leak channels), initiating a positive feedback loop (rising phase). At around +40 mV the voltage gated sodium channels begin to close (peak phase) and the voltage gated potassium channels begin to open, moving potassium against its electrochemical gradient and out of the cell (falling phase). The potassium channels exhibit a delayed reaction to the membrane repolarisation, and even after the resting potential is achieved, some potassium continues to flow out, resulting in an intracellular fluid which is more negative than the resting potential, and during which, no action potential can begin (undershoot phase). This undershoot phase ensures that the action potential propagates down the axon and not back up it. Once this initial action potential is initiated, principally at the axon hillock, it propagates down the length of the axon. Under normal conditions, the action potential would attenuate very quickly due to the porous nature of the cell membrane. To ensure faster and more efficient propagation of action potentials, the axon is myelinated. Myelin, a derivative of cholesterol, acts as an insulating sheath and ensures that the signal can not escape through the ion or leak channels. There are, nevertheless, gaps in the insulation (nodes of ranvier) which boost the signal strength. As the action potential reaches a node of Ranvier, it depolarises the cell membrane. As the cell membrane is depolarised, the voltage gated sodium ions open and sodium rushes in, triggering a fresh new action potential.

See also Initiation Action


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