Primary sensory afferents contain GABA receptors along their terminals (reviewed in:, Table 1). GABA receptors are ligand-gated chloride channels, formed by the assembly of five GABA receptor subunits. In addition to the presence of GABA receptors along sensory afferent axons, the<unk>  terminal also has a distinct ionic composition that is high in chloride concentration. This is due to cation-chloride cotransporters (for example, NKCC1) that maintain highs intracellular chloride. Typically when GABA receptors are activated, it causes a chloride influx, which hyperpolarizes the cell. However, in primary afferent fibers, due to the high concentration of chloride at the<unk>  terminal and thus its altered reversal potential, GABA receptor activation actually results in a chloride efflux, and thus a resulting depolarization. This phenomenon is called primary afferent depolarization (PAD). The GABA-induced depolarized potential at afferent axons has been demonstrated in many animals from cats to insects. Interestingly, despite the depolarized potential, GABA receptor activation along the axon still results in a reduction of neurotransmitter release and thus still is inhibitory. There are four hypotheses which propose mechanisms behind this paradox: # The depolarized membrane causes inactivation of voltage-gated sodium channels on the terminals and therefore the action potential is prevented from propagating. # Open GABA receptor channels act as a shunt, whereby current is dissipated of instead of being propagated to the terminals. #The depolarized membrane causes inactivation of voltage-gated calcium channels, preventing calcium influx at the synapse (which is imperative for neurotransmission). #The depolarization at the terminals generates an antidromic spike (i.e. an action potential generated in the axon and travels towards the soma), which would prevent orthodromic spikes (i.e. an action potential traveling from the cell's soma toward the axon terminals) from propagating.
Presynaptic inhibition
Neural facilitation
Paraspinal inhibition
Neural adaptation
Co-stimulation
Spike-timing-dependent plasticity
Lateral inhibition
Cortical remapping