Abstract
Inhibitory neurotransmission in the spinal dorsal horn is at the foundation of the Gate Control Theory of Pain and has been the subject of intense investigation [16; 21]. The dorsal horn is richly endowed with GABAergic and glycinergic neurons and their ionotropic receptors. GABAA receptors are located presynaptically on afferent terminals and both glycine and GABAA receptors are found postsynaptically on dorsal horn neurons [15]. Pharmacologically blocking those receptors can reproduce many features of persistent pain, including mechanical allodynia and spontaneous pain. There is now unequivocal evidence that inhibition in the spinal dorsal horn is pathologically reduced after peripheral nerve injury and persistent inflammation [6; 12; 14]. Importantly, disinhibition can develop via distinct mechanisms. Here we concisely review how disinhibition occurs, focusing on mechanisms affecting postsynaptic inhibition in dorsal horn neurons. We also discuss emerging therapeutic opportunities to restore normal inhibition.
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