Showing papers on "Rapid eye movement sleep published in 1971"
TL;DR: The generality of these findings was obtained by depriving mice of REM sleep during the interval between a discrimination training experiment in a black-white T-maze and the subsequent retention test, which showed a temporary retrograde amnesia.
144 citations
TL;DR: The results suggest that PGOW and PGOREM are closely related, but not identical, phenomena, both dependent upon the activity of pacemakers localized in the pons.
98 citations
TL;DR: Five days of REM sleep deprivation in the rat produced marked acquisition deficits which were not task specific and which did not appear to be due to nonspecific stress, non-REM sleep loss, or changes in activity levels.
88 citations
TL;DR: Mice that were deprived of rapid eye movement sleep for 2 days immediately after one-trial training in an inhibitory avoidance task and were given an electroconvulsive shock after deprivation displayed retrograde amnesia on a retention test given 24 hours later.
Abstract: Mice that were deprived of rapid eye movement sleep for 2 days immediately after one-trial training in an inhibitory avoidance task and were given an electroconvulsive shock after deprivation displayed retrograde amnesia on a retention test given 24 hours later. Electroconvulsive shock produced no amnesia in comparable groups of animals that were not deprived of rapid eye movement sleep.
70 citations
TL;DR: Absence of the peak of plasma growth hormone levels normally seen following the onset of sleep was observed in five blind subjects, and subjects displayed a decreased amount of slow wave sleep and an increase in time spent in combined stages I, II and rapid eye movement sleep.
Abstract: Absence of the peak of plasma growth hormone levels normally seen following the onset of sleep was observed in five blind subjects. These subjects also displayed a decreased amount of slow wave sleep (stages III and IV) and an increase in time spent in combined stages I, II and rapid eye movement sleep. Insulin hypoglycemia produced a normal rise in plasma growth hormone levels in three subjects so tested.
41 citations
TL;DR: This chapter discusses the pharmacology of rapid eye movement sleep, a rhythmical and temporary interruption of wakefulness, induced by internal, not external, factors, in which consciousness of environmental features subsides to a minimum.
Abstract: Publisher Summary This chapter discusses the pharmacology of rapid eye movement sleep. Sleep is rest, quiescence, a time when bodily functions subside to a low point. Its purpose is surcease and restoration. Sleep can be defined as a rhythmical and temporary interruption of wakefulness, induced by internal, not external, factors, in which consciousness of environmental features subsides to a minimum; in which movement of the body is almost completely absent; in which there is an increase in the thresholds of reactivity and of reflex irritability; in which there occurs a continuum which leads from light sleep to deep sleep; in which there occurs, also, a rhythmical alternation of this light sleep-deep sleep cycle; in which at the peak of each of these cycles, certain functions become accelerated and, at least in the human, there occurs the phenomenon of dreaming; and in which there exists a built-in mechanism which after a time produces the phenomenon of arousal.
36 citations
TL;DR: It is suggested that the neural mechanism of the depression of the Babinski reflex during REM may be different from that operating in the waking state, and that the suppression is caused by influences descending from supraspinal centers to the reflex arc of the babinski reflex.
24 citations
01 Jan 1971
21 citations
01 Jan 1971
TL;DR: Although there have been many good reasons to look for a brain indoleamine N-methylating enzyme since the introduction of the Harley-Mason amine methylation hypothesis of schizophrenia, the interests of this author in this field started in 1964 when he was studying the effect of the intravenous infusion of various amine precursors on sleep patterns in man.
Abstract: Although there have been many good reasons to look for a brain indoleamine N-methylating enzyme since the introduction of the Harley-Mason amine methylation hypothesis of schizophrenia (Osmond and Smythies 1952) and Axelrod’s exciting and systematic elucidation of various amine-methylating enzymes in the central nervous system (Axelrod 1965), our own particular interests in this field started in 1964 when we were studying the effect of the intravenous infusion of various amine precursors on sleep patterns in man. We reported a 5-hydroxytryptophan (5-HTP)-induced increase in rapid eye movement sleep (Mandell, Mandell, and Jacobson 1965). At the same time we noted that occasionally there was a disruption of sleep during 5-HTP infusions, with episodes of bizarre mentation. Whereas 5-hydroxytryptophan alone in small doses (150 mg i.v. over 6 to 8 hours) would usually produce some degree of sedation in our subjects, higher doses (200 mg or more), or smaller doses given in combination with a monoamine oxidase inhibitor as a pretreatment before intravenous amino acid load produced behavioral and psychic activation. We then became aware of the wide variety of studies by a number of investigators (Kety 1961; Pollin, Cardon, and Kety 1961; Kline, Simpson, and Sacks 1967; Himwich et al. 1970) that demonstrated similar reversals of the indoleamino acid-produced sedation with monoamine oxidase inhibitor pretreatment.
9 citations