Neural backpropagation

Moreover, the voltage-gated sodium channels on the dendritic membranes having a higher threshold helps prevent them triggering an action potential from synaptic input.

This impulse travels up the axon eventually causing the cell body to become depolarized, thus triggering the dendritic voltage-gated calcium channels.

It is thought that this is due to the fact that each neuronal cell type contains varying numbers of the voltage-gated channels required to propagate a dendritic action potential.

Typically, they play a crucial role in returning the cell to its resting membrane following an action potential by allowing an inhibitory current of K+ ions to quickly flow out of the neuron.

Additionally, the presence of these channels provides a mechanism by which the neuron can suppress and regulate the backpropagation of action potentials through the dendrite (Vetter 2000).

Pharmacological antagonists of these channels promoted the frequency of backpropagating action potentials which demonstrates their importance in keeping the cell from excessive firing (Waters et al., 2004).

Essentially, inhibition occurs because the A-type channels facilitate the outflow of K+ ions in order to maintain the membrane potential below threshold levels (Cai 2007).

Such inhibition limits EPSP and protects the neuron from entering a never-ending positive-positive feedback loop between the soma and the dendrites.

The backpropagating current also causes a voltage change that increases the concentration of Ca2+ in the dendrites, an event which coincides with certain models of synaptic plasticity.

Neural backpropagation occurs in this window to interact with NMDA receptors at the apical dendrites by assisting in the removal of voltage sensitive Mg2+ block (Waters et al., 2004).

Current literature also suggests that backpropagating action potentials are also responsible for the release of retrograde neurotransmitters and trophic factors which contribute to the short-term and long-term efficacy between two neurons.

Moreover, backpropagating action potentials have been shown to induce BDNF-dependent phosphorylation of cyclic AMP response element-binding protein (CREB) which is known to be a major component in synaptic plasticity and memory formation (Kuczewski N., Porcher C., Lessmann V., et al. 2008).