抄録
Disinhibition such as a loss of inhibitory interneurons or a shift in the transmembrane anion gradient especially in the substantia gelatinosa (SG) of the spinal dorsal horn is thought to be a crucial etiology for chronic pain syndromes. However, there is little direct evidence to elucidate the natural inhibitory mechanism for nociceptive transmission because of difficulties in recording inhibitory synaptic responses from small size SG neurons in vivo. In this study, whole-cell recordings were obtained from SG neurons in vivo and in slice preparations to analyze how inhibitory synaptic inputs modulate noxious transmission and the underlying neuronal circuits. SG neurons in vivo responded to cutaneous pinch accompanied with a barrage of EPSCs. On the other hand, touch evoked a barrage of IPSCs during the stimulation and the receptive fields were larger than those of pinch-evoked EPSCs. After cessation of a brief touch, a burst of IPSCs lasted for about 10 s in some cells. The number of action potentials generated by pinch was decreased by the simultaneous stimulation of touch applied to the surrounding area. In slice experiments, activation of C fiber was required to elicit the burst of inhibitory response and large islet cells known as an inhibitory interneuron received C fiber inputs. The results suggest that innocuous stimulation even brief touch sufficiently suppresses noxious sensation in the SG through activation of C fibers. [J Physiol Sci. 2006;56 Suppl:S21]
