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D Psatta

Publications and source records attributed to D Psatta.

9 recordsLinked to original sources

Sleep in the cat: raphe dorsalis and vasotocin.

To determine the relationship between the raphe nuclei and the sleep-inducing 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 (RDN) or the raphe pontis nucleus (RPN). The following results were observed: (a) RDN 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) RDN 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 RDN; (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) RDN 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.

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Slow-wave sleep induced in cats by extremely small amounts of synthetic and pineal vasotocin injected into the third ventricle of the brain.

A single injection of 10(-6) pg synthetic arginine vasotocin (AVT), corresponding to about 600 molecules AVT, into the third ventricle of unanesthetized cats, induced slow-wave sleep 5 min after the injection. An equivalent amount, of a partially purified pineal AVT injected into the third ventricle, produced the same effects. After incubation with trypsin, pineal AVT completely lost its ability to induce slow-wave sleep. The slow-wave sleep induced by 10(-6) pg synthetic AVT injected intraventricularly could be matched by 1 microgram synthetic AVT injected intraperitoneally. Neither synthetic arginine vasopressin, nor synthetic oxytocin, injected intraventricularly in the amount of 10(-6) pg, was able to induce slow-wave sleep. Whereas in the control animals injected with pineal AVT after incubation with trypsin, or in the control animals injected with vasopressin or oxytocin, the paradoxical sleep averaged 21.9--22.8% of the sleep time, during a total recording time of 5 hr, in the cats injected with synthetic or pineal AVT, the paradoxical sleep was completely suppressed.

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REM sleep rebound after its suppression by vasotocin in cats.

Extremely small amounts (10(-4) pg) of synthetic arginine vasotocin (AVT) injected into the pineal recess of unanesthetized cats induced a continuous NREM sleep for about 60 minute and completely suppressed REM sleep for about 5 hours. The reappearance of the REM sleep following AVT administration occurred with a marked rebound, lasting for more than one hour. Since neither vasopressin nor oxytocin, at the same doses, were able to affect significantly the REM sleep, it is concluded that AVT is specifically involved in the modulation and/or circadian organization of the REM sleep.

Animals↗