Neurotransmission by neurons that use serotonin, noradrenaline, glutamate, glycine, and gamma-aminobutyric acid in the normal and injured spinal cord.

Abstract

The science of neurotransmission in the normal and injured spinal cord has grown. This is a review of neurotransmission using serotonin, noradrenaline, glutamate, glycine, and gamma-aminobutyric acid. The literature on spinal cord neurotransmission and changes that occur with trauma are reviewed. Serotonergic and noradrenergic bulbospinal tracts influence interneurons and motor neurons via postsynaptic inhibition. Colocalization of serotonin and thyrotropin-releasing hormone occur in bulbospinal tracts, and reduction in uptake and thyrotropin-releasing hormone immunoreactivity quantitates the degree of injury in chronic spinal cord injury (SCI). Glutamate functions as an excitatory transmitter of some dorsal root afferent neurons and interneurons modulating nociceptive and motor neurons via at least five different receptors. Reactive synaptogenesis occurs after SCI, leading to an increase in the number of excitatory glutamatergic synapses below the level of SCI. gamma-Aminobutyric acid is an inhibitory transmitter of spinal interneurons that functions both pre- and postsynaptically. After SCI, a reduction occurs in the number of inhibitory synapses related to gamma-aminobutyric acid. Glycine is an inhibitory neurotransmitter that functions postsynaptically and also modulates the N-methyl-D-aspartate receptor. After SCI, a reduction in glycine adds to the loss of local inhibition below the SCI.