Central Transmitter Action

Glutamate is the major transmitter released onto spinal neurons by nociceptive afferents. It activates AMPA-kainate receptors on central neurons to produce rapid EPSPs that excite them. This system is responsible for the rapid, nonpersisting pain acting as a signal to the organism to remove the stimulated tissue from the potentially damaging stimulus.

Cells in the superficial dorsal horn also express another glutamate receptor known as the N-methyl-d-aspartate (NMDA) receptor, whose activation can lead to long-lasting activity and extensive metabolic changes in these cells, resulting in persistent pain.

Activation of these receptors is facilitated by corelease of peptides, particularly substance P, from terminals of the afferent fibers in response to intense activity. Substance P elicits a long, slow depolarization of its target cells via activation of tachykinin (NK1) receptors. This depolarization acts to remove the block of postsynaptic NMDA receptors that occurs in the presence of extracellular Mg at normal resting potentials. The details of pre- and postsynaptic changes in central neurons as a consequence of activation of NMDA receptors as well as the interaction between these neural elements in eliciting these long-term changes are presently not completely characterized. Not all nociceptive afferents may be able to elicit long-term changes in this manner because many IB4/c-ret/ FRAP-expressing nociceptive afferents are not peptidergic.

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