OBJECTIVE: The science of neurotransmission in the normal and injured spinal curd has grown. This is a review of neurotransmission using serotonin, noradrenaline, glutamate, glycine, and γ-aminobutyric acid. METHODS: The literature on spinal cord neurotransmission and changes that occur with trauma are reviewed. CONCLUSION: 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. γ-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 γ-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.
- γ-Aminobutyric acid spinal neurotransmission
- Glutamate, spinal neurotransmission
- Glycine spinal neurotransmission
- Serotonin spinal neurotransmission
- Spinal cord injury
ASJC Scopus subject areas
- Clinical Neurology