Summary: To determine the relationship between the raphe nuclei and the sleepinducing pineal peptide arginine vasotocin (AVT), we investigated the hypnogenic effects of intraventricularly administered AVT in adult cats with electrolytic lesions performed either in the raphe dorsalis nucleus (RON) or the raphe pontis nucleus (RPN). The following results were observed: (a) RON lesions produced a quantitative decrease in NREM sleep and a transitory increase in REM sleep and narcoleptic-like alterations of REM sleep in the first 2-5 postoperative days. On the eighth postoperative day, normal (prelesion) sleep parameters were restored. (b) RON lesions prevented AVT from inducing its hypnogenic effects during the first 5 postoperative days, but the AVT hypnogenic effects reappeared when sleep parameters reached prelesion levels. (c) Although the RPN lesions produced a slight but statistically significant REM sleep decrease, this did not prevent AVT from inducing its hypnogenic effects. We conclude that (a) the anatomic site of AVT action within the brain may be related to RON; (b) at least some of the sleep disturbances observed after RDN lesions (narcolepsy) may be due to damage of the AVT site of action or to modifications of AVT synthesis or release; (c) RON belongs to a large neural circuit that includes the pineal gland and habenula, a circuit that may play an important role in the sleep-wake cycle by "fine-tuning" sleep mechanisms. We hypothesize that AVT could be the specific inhibitory neuromodulator of this neural circuit. Key Words: Vasotocin---NREM sleep---REM sleep---Raphe dorsalis-Raphe pontis.The pineal nonapeptide hormone arginine vasotocin (AVT) is synthesized by specialized ependymal cells from the pineal recess and subcommissural organ (1) and released into cerebrospinal fluid in man during REM sleep (2,3) and in the cat after lateral habenula lesions (4). The effects of AVT on mammalian sleep are controversial, results varying from an enhancement of NREM sleep and a suppression of REM sleep in cats (5) to an increase of REM sleep in man (6), and from a reduction of REM sleep latency (7) or reduction in the power of the delta band of electrocorticograms (8) to reduction of REM sleep in the light-phase (9,10) and suppression of REM sleep in the dark-phase of the 24 h period (9) in the rat. The serotonin-containing neurons, for which involvement in the sleep-wake cycle
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