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Biomedical subjects

N Sitaram

Publications and source records attributed to N Sitaram.

At least 73 records · Page 4Linked to original sources
PubMed1981

Physostigmine induction of depressive symptomatology in normal human subjects.

Nine normal volunteers, screened for the absence of a personal or family history of affective disorders and free of concurrent marijuana usage, received intravenous infusions of high dose physostigmine or saline in a randomized, double-blind, counterbalanced paradigm. Self-rating and observer ratings both demonstrated a statistically significant, physostigmine associated increase in depressive-type symptoms in the group as a whole, particularly pronounced in certain individuals. These results are the first report of physostigmine associated depressive symptomatology in normal subjects. While our findings are discrepant with two previous studies, our use of multiple self-ratings, and some differences in physostigmine dosage and infusion times might have contributed to this difference. These findings suggest that high dose physostigmine may represent a pharmacological model of depression in normal subjects, or alternatively may be diagnostic of vulnerability to affective disorder in certain subjects free of a previous history of affective disturbances.

Adolescent↗
PubMed1980

Faster cholinergic REM sleep induction in euthymic patients with primary affective illness.

Arecoline, a cholinergic muscarinic receptor agonist, induced rapid eye movement sleep significantly more rapidly in patients with primary affective illness in remission than in normal control subjects matched for age and sex. These results, and others, suggest that patients with primary affective illness may have a supersensitive cholinergic system both when they are ill and when their symptoms are in clinical remission.

Adult↗
PubMed1980

Development and use of pharmacological probes of the CNS in man: evidence of cholinergic abnormality in primary affective illness.

The role of cholinergic mechanisms in the regulation of CNS functions was studied in normal humans. The purpose was to develop in vivo pharmacological techniques to assess central neurotransmitter activity in normals and apply them in primary affective illness and other neuropsychiatric conditions. Central cholinergic stimulation by cholinomimetics induced rapid eye movement (REM) sleep, dreaming, cortical arousal, and accelerated the REM cycle. Effects on memory included enhancement of serial learning, short-term consolidation of low-imagery words, and retrieval of clustered information. Analgesia and reduction of the P100 component of visual EEG evoked responses were also noted after physostigmine. Using the induction of REM sleep by arecoline as a "marker" of central cholinergic functioning, it was possible to (i) demonstrate the phenomenon of pharmacological denervation supersensitivity in normal humans after pretreatment with scopolamine, and (ii) demonstrate a significantly faster REM induction by arecoline in two groups of patients with primary affective illness (remitted and depressed) compared to normals. Rapid REM induction was found, not only in remitted patients who were drug-free for 2 weeks, but in patients who had never received somatic therapy. Pretreatment with scopolamine on three consecutive mornings also induced sleep changes at night in normals similar to several sleep abnormalities reported in primary affective illness. This was confirmed by a multivariate discriminate analysis program, which had previously been shown to separate depressed patients, insomniacs, and normals. On the basis of these data, it is proposed that cholinergic abnormalities may be present in primary affective illness during both the ill and the well states.

Acetylcholine↗
PubMed1979

Scopolamine-induced muscarinic supersensitivity in normal man: changes in sleep.

Scopolamine (6 microgram/kg) was administered on 3 consecutive mornings to normal human subjects. Sleep recordings obtained at night (when the central anticholinergic effect of the morning scopolamine was no longer present) indicated a significant reduction in latency to REM-sleep onset on the nights following the second and third injections. This effect is opposite to the direct pharmacological action of nighttime administration of scopolamine (i.e., prolongation of REM latency). In addition, total sleep time and sleep efficiency were reduced, and sleep latency was increased. Furthermore, scopolamine pretreatment on 2 consecutive mornings also potentiated the REM-inducing effect of arecoline, a central muscarinic agonist. These data are consistent with the development of cholinergic supersensitivity following cholinergic blockade.

Adult↗
PubMed1979

Muscarinic supersensitivity: a possible model for the sleep disturbance of primary depression?

The sleep changes induced in normal volunteers following the administration of scopolamine on 3 consecutive mornings resemble many of the abnormalities observed in the sleep of patients with primary depression: increased sleep latency and reduced rapid eye movement (REM) latency, total sleep time, and sleep efficiency. Furthermore, in a multivariate discriminant analysis--previously shown to distinguish the sleep records of depresed patients from those of normal controls and insomniac patients--the records from baseline nights were selected as normal and those after scopolamine as predominately depressed. Those observations suggest to us that muscarinic supersensitivity in normals may function as a pharmacological model for the sleep disturbances of depression.

Depression↗
PubMed1978

Human serial learning: enhancement with arecholine and choline impairment with scopolamine.

Arecholine (4 milligrams), a cholinergic agonist, and choline (10 grams), a precursor of acetylcholine, significantly enhanced serial learning in normal human subjects. The subjects received methscopolamine prior to both arecholine and placebo injections. Conversely, scopolamine (0.5 milligram), a cholinergic antagonist, impaired learning and this impairment was reversed by arecholine and choline and the impairment after scopolamine were inversely proportional to the subject's performance on placebo; that is, "poor" performers were more vulnerable to both the enhancing effect of cholinergic agonist and precursor and the impairment after cholinergic antagonist than "good" performers.

Acetylcholine↗
PubMed1978

Physostigmine alters onset but not duration of REM sleep in man.

Physostigmine (1.0mg) or placebo were administered intravenously over 1-h period to seven male normal volunteers beginning 35 min after sleep onset. The results indicate that physostigmine induced the onset of REM sleep but did not significantly alter the duration of individual REM sleep periods. Physostigmine significantly shortened the REM latency and the duration of the second nonREM period. After inducing the onset of the first REM period(s); physostigmine also appeared to advance succeeding REM-nonREM sleep cycles relative to sleep onset even when the duration of each cycle was unaffected.

Adult↗
PubMed1978

The effect of physostigmine on normal human sleep and dreaming.

Physostigmine, an anticholinesterase that increases the action of brain acetylcholine, induces rapid eye movement (REM) sleep in normal humans. In this study we show that man dreams during physostigmine-induced REM sleep. Seventeen normal volunteers were pretreated with methscopolamine and received one intravenous infusion per night of either placebo or physostigmine either ten or 35 minutes after sleep onset. Subjects were awakened at specific times after infusion and interviewed regarding any sleep mentation prior to awakening. Results indicated that dreaming occurred during physostigmine-induced REM periods but that physostigmine did not alter mentation during non-REM sleep. These dreams were similar to spontaneous REM sleep dreams in content, vividness, unusualness, and emotionality.

Adult↗
PubMed1978

Induction and resetting of REM sleep rhythm in normal man by arecholine: blockade by scopolamine.

Arecholine, a cholinergic muscarinic agonist, was administered intravenously 35 min after sleep onset in eight normal volunteers who had been pretreated with either methscopolamine or scopolamine, muscarinic receptor blockers that do not and do cross the blood--brain barrier, respectively. Following pretreatment with methscopolamine, arecholine shortened the REM latency and increased the number of REM periods without altering the duration of individual REM periods or altering the REM--REM intervals. Pretreatment with scopolamine blocked the effects of arecholine. The results support the hypothesis that cholinergic muscarinic mechanisms are involved in the timing but not the duration of REM sleep.

Adult↗