[Involvement of serotoninergic systems in analgesia induced by electrical stimulation of brain stem areas (author's transl)]

Numerous studies in the rat have shown that powerful analgesia can be induced by electrical stimulation of the periaqueductal grey matter (PGM). From an extensive mapping (300 sites of stimulation) performed on unrestrained cats, we have demonstrated that the points from which analgesia can be obtained are essentially located in the raphe nuclei: dorsal raphe nucleus (DRN) located in the ventral part of the PGM, superior part of the nucleus central superior (CS) and nucleus central inferior (mainly the raphe magnus: RM). The most powerful effects were induced by stimulation sites located in the RM. At this level, similar findings were also obtained in the rat. Accumulating evidence suggests that electrical analgesia (EA) results, partly, from the activation of bulbospinal systems which block the transmission of noxious messages at the spinal level: (a) Spinal cord nociceptive reflexes and jaw-opening reflex induced by tooth pulp stimulation are suppressed by EA. (b) Responses of dorsal horn neurons to noxious stimuli are drastically reduced by PGM and RM stimulations; similar findings have been reported for trigeminal neurons in the nucleus caudalis. (c) Neurons at the origin of the spinothalamic tract in the monkey or at the origin of the spinoreticular tract in the rat are strongly inhibited by RM stimulation. These electrophysiological results are in agreement with anatomical data showing that RM has dense projection at the level of the dorsal horn. All these results clearly demonstrate that the raphe nuclei, rich in serotoninergic cell bodies, seem to play a basic role in the mechanism of electrical analgesia. The involvement of serotonin is strongly suggested by numerous behavioral, electrophysiological, anatomical and neurochemical investigations. In addition, PGM and RM are strongly implicated in morphine analgesia which has several common characteristics with EA. The most striking evidence results from the observation that EA is decreased or suppressed after administration of an opiate antagonist (Naloxone). This observation suggests that electrical stimulation releases morphine-like endogenous substances.