![]() ![]() This is consistent with observations that synaptic plasticity is much more apparent in areas like the hippocampus, which controls memory, than the cerebellum, which controls more unconscious and vegetative functions. On average, a backpropagating spike loses about half its voltage after traveling nearly 500 micrometres.īackpropagation occurs actively in the neocortex, hippocampus, substantia nigra, and spinal cord, while in the cerebellum it occurs relatively passively. It is also dependent on the shape of the dendritic tree and, more importantly, on the rate of signal currents to the neuron. This current decays significantly with travel length along the dendrites, so effects are predicted to be more significant for neurons whose synapses are near the postsynaptic cell body, with magnitude depending mainly on sodium-channel density in the dendrite. Since the 1950s, evidence has existed that neurons in the central nervous system generate an action potential, or voltage spike, that travels both through the axon to signal the next neuron and backpropagates through the dendrites sending a retrograde signal to its presynaptic signaling neurons. EPSPs from synaptic activation are not large enough to activate the dendritic voltage-gated calcium channels (usually on the order of a couple milliAmps each) so backpropagation is believed to happen only when the cell is activated to fire an action potential. Voltage-gated calcium channels can then lead to a propagating (most of the time) dendritic action potential. However, the cell body or soma can also become depolarized when an action potential is initiated, and this depolarization can spread out to the dendritic tree where there are voltage-gated calcium channels. ![]() An action potential spreads down the axon because of the gating properties of voltage-gated sodium channels and voltage-gated potassium channels. When a neuron fires an action potential, it is initiated at the axon hillock. ![]()
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