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Axonal and somato‐dendritic modalities of serotonin release: their involvement in sleep preparation, triggering and maintenance
Author(s) -
CESPUGLIO R.,
HOUDOUIN F.,
OULERICH M.,
MANSARI M. EL,
JOUVET M.
Publication year - 1992
Publication title -
journal of sleep research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.297
H-Index - 117
eISSN - 1365-2869
pISSN - 0962-1105
DOI - 10.1111/j.1365-2869.1992.tb00030.x
Subject(s) - sleep (system call) , neuroscience , serotonin , neuroscience of sleep , stimulation , rapid eye movement sleep , slow wave sleep , postsynaptic potential , psychology , chemistry , medicine , electroencephalography , receptor , computer science , operating system
SUMMARY SUMMARY That serotonin (5‐HT) plays a determinant role in sleep was first suggested by the well‐known PCPA‐5HTP (p.chlorophenylalanine‐5‐hydroxytryptophan) paradigm. This involvement, however, is paradoxical since localized cooling of the nucleus raphe dorsalis (n.RD) is sleep inducing, and unitary activity of 5‐HT neurons decreases during slow wave sleep (SWS) and paradoxical sleep (PS). Furthermore, on the basis of voltammetric 5‐hydroxyindole (5‐OH lcs ) measurements, it appears that 5‐HT could be released throughout the sleep/wake cycle according to two different modalities: by the axonal nerve endings during the waking state (W) and by the dendrites and/or the soma during sleep. The axonal release of 5‐HT might participate in sleep preparation by stimulating the synthesis of hypnogenic factors within target structures like the basal hypothalamus (BH). When such a release is increased by an immobilization stress (IS) or electrical stimulation of the n.RD, a sleep rebound is induced. The somato‐dendritic release of 5‐HT might be primarily responsible through an auto‐inhibitory process for the decrease and abolition of the 5‐HT neuronal unitary activity as well as for the reduction of the axonal release of 5‐HT; both phenomena being constantly observed during sleep. Finally, the hypnogenic factors might initiate and maintain sleep by influencing the n.RD sleep gating mechanisms either through the somato‐dendritic release of 5‐HT, or directly.