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Biomedical subjects

J C Gillin

Publications and source records attributed to J C Gillin.

At least 199 records · Page 11Linked to original sources
PubMed1983

Hypnogenic center theory of sleep: no support from metabolic mapping in monkeys.

By comparing rates of glucose utilization in brains of monkeys in non-REM sleep and two types of awake controls, we attempted to reveal cerebral hypnogenic centers that drive organisms to sleep through increases in their neural activity. Instead we found that metabolic activity is reduced in all the putative hypnogenic centers during sleep as compared to wakefulness. The results thus offer no support for the notion of an active center that either maintains or triggers sleep.

Animals↗
PubMed1983

Behavioral, physiological, and neuroendocrine responses to arecoline in normal twins and "well state" bipolar patients.

Cholinergic supersensitivity has been postulated to be an etiologic factor in affective disorder. After several pilot dose-response studies, we administered 8 mg of the cholinergic agonist arecoline subcutaneously to eight pairs of normal volunteer identical twins and eight bipolar patients currently euthymic and unmedicated. During the hour following arecoline administration, the Profile of Mood States (POMS) showed an increase in total mood disturbance in both patient and control groups. Mean systolic blood pressure, pulse, plasma cortisol, prolactin, and growth hormone also increased. Anger and elation scores on the POMS showed significant concordance in identical twins, as did change in prolactin, implying that these are the components of drug response possibly influenced by genetic factors. None of these responses differentiated well state patients from controls. Thus, mood, behavioral, and neurochemical responses to arecoline, which appears to have nonspecific neurochemical effects at the dose employed, are not markers of vulnerability to affective illness.

Arecoline↗
PubMed1983

Adrenergic-cholinergic balance and the treatment of affective disorders.

Centrally acting cholinomimetic drugs cause anergia, behavioral inhibition and depression. Centrally acting cholinomimetic drugs have antimanic properties. Combinations of acetylcholine precursors and centrally active cholinomimetic agents may cause augmented muscarinic effects, as may a combination of an antiadrenergic and cholinomimetic drugs. Centrally active anticholinergic agents may exert antidepressant effects. Affective disorder patients may show hyperreactivity to cholinomimetic agents, a phenomena which may have diagnostic significance.

Acetylcholine↗
PubMed1983

The sleep therapies of depression.

This paper reviews five different types of deliberate sleep-wake manipulations which are reported to have antidepressant effects: total sleep deprivation, partial sleep deprivation, a phase advance of the sleep periods, and REM deprivation. The effects of total sleep deprivation are best documented. Of 852 depressed patients studied, 493 or 57.9% improved following sleep deprivation. The REM deprivation procedure acts more slowly, but is of more lasting clinical value than the other forms. Partial sleep deprivation during the second half of the night may be as good as total sleep deprivation and better tolerated. The findings are reviewed in terms of psychological, neurophysiological, biochemical, and chronobiological perspectives.

Depressive Disorder↗
PubMed1983

Successful treatment of human non-24-hour sleep-wake syndrome.

The authors report a case in which a non-24-h (hypernychthemeral) sleep-wake cycle appeared as a late complication of a more fundamental disturbance in the quality of sleep (difficulty falling asleep, frequent awakenings, nonrefreshing sleep). The sleep disturbance began abruptly after a series of stressful events. The patient reported that he extended his hours of bedrest in the morning in order to increase his total sleep time and feel mor rested, and that he gradually extended his hours of activity in the late evening in order to increase his drowsiness and ability to fall asleep. At first this behavior, which was a deliberate attempt to compensate for inefficient nighttime sleep, led to a delayed sleep period, as also occurs in the delayed sleep phase syndrome. After several years in which sleep efficiency progressively deteriorated, this behavior led to a non-24-h free-running sleep-wake cycle. After the patient was treated with thyroxine for borderline hypothyroidism, and then flurazepam and finally vitamin B12, his sleep disturbance progressively improved and his sleep-wake cycle shortened. After B12 treatment he was able to advance the timing of ;his sleep period for the first time in nearly 10 years and to follow a normal 24-h sleep-wake regimen.

Adult↗
PubMed1983

CSF copper concentrations in chronic schizophrenia.

The authors used a sensitive flameless atomic absorption spectrophotometric procedure to measure CSF copper concentrations in normal controls, former heroin addicts, and unmedicated and medicated chronic schizophrenic patients and found no significant differences in CSF copper levels between these groups. Schizophrenic women had significantly lower CSF copper levels than schizophrenic men, but no significant differences were found between control men and control women. There were no differences in CSF copper levels between patient subgroups with respect to diagnostic subtype (acute versus chronic, paranoid versus chronic undifferentiated), length of hospitalization, race, medication status, platelet monoamine oxidase values, or CAT scan abnormalities.

Adult↗
PubMed1983

Negative feedback suppression of sleep-related growth hormone secretion.

Previous studies have demonstrated that injections of growth hormone (GH) can blunt subsequent GH secretory responses to daytime pharmacological stimulation. The current study was undertaken to determine whether GH administration to normal subjects would suppress sleep-related secretion. GH (2 U im) was given nine times over 5 days to each of six subjects, and sleep studies with blood sampling were performed 6 h after the last injection. Secretion during the first 2 h of sleep was decreased by 62.4%, indicating that sleep-related GH secretion may be responsive to a negative-feedback mechanism.

Adult↗
PubMed1983

A twin study of cholinergic REM induction.

Seven monozygotic twin pairs were found to display concordance for sensitivity to REM sleep induction by arecoline (intraclass correlation (ri) of 0.69, F = 5.35, p less than 0.02). The REM1-REM2 interval on the placebo night did not show significant concordance (ri = 0.05, F = 1.11, p = 0.44). Our previous study suggested that increased sensitivity to the muscarinic agonist arecoline, as measured by time to onset of the second REM period during sleep, may be an indicator of vulnerability to affective disorder. The present finding of twin concordance in response to arecoline suggests genetic variation in sensitivity of CNS muscarinic cholinergic receptors. Such increased sensitivity may play an etiologic role in affective disorder.

Adolescent↗
PubMed1983

Circadian rhythm disturbances in manic-depressive illness.

Clinical features of manic-depressive illness, such as diurnal variation in mood, early morning awakening, and cyclicity and seasonality of recurrences, have led to speculation that the circadian system may be involved in its pathophysiology. At least three types of circadian rhythm abnormalities have been described in such patients: blunting of circadian rhythms' amplitudes, advanced position (or even nonentrainment) of circadian rhythms' phases, and doubling of the length of the sleep-wake cycle from 24 to 48 h. Several types of experiments indicate that alterations in the timing of sleep and wakefulness relative to other circadian rhythms (i.e., changes in internal phase relationships) may trigger the onset or offset of episodes of depression and mania. Whether drugs used to treat manic-depressive illness act through their effects on the circadian system is currently being investigated. Direct manipulations of the circadian system are also being investigated as new approaches to treatment.

Bipolar Disorder↗
PubMed1982

The effect of naloxone on normal human sleep.

Placebo and naloxone (4, 8, and 12 mg) were infused on separate nights in a double-blind fashion over a 20-min period between the 25th and 45th min of sleep in normal volunteers. Naloxone produced a dose-dependent increase in REM latency (the time from onset of sleep until the first REM period), and duration of the first REM period and second NREM period. The number of REM periods was also reduced.

Dose-Response Relationship, Drug↗
PubMed1982

Plasma prolactin concentrations and psychopathology in chronic schizophrenia.

Plasma prolactin concentrations in 17 drug-free chronic schizophrenic patients correlated inversely with ratings of their psychopathology. An inverse relationship between psychotic symptoms and plasma prolactin concentrations was particularly clear in patients with normal cerebral ventricular size as determined by computed tomography. The psychosis-prolactin relationship did not hold for schizophrenic patients with large ventricular size. These data suggest that the degree of psychosis is related to dopaminergic activity insofar as this is reflected by plasma prolactin concentrations, especially in schizophrenic patients with normal ventricular size. These findings lend further support to the hypothesis that ventricular size is a meaningful factor in subtyping chronic schizophrenic patients.

Adult↗
PubMed1982

The sleep of patients with obsessive-compulsive disorder.

Fourteen patients with obsessive-compulsive disorder (OCD) were studied with all-night sleep EEG recordings. Nine of these patients reported abnormal sleep patterns before the polygraphic study. Analysis of the sleep records disclosed significantly decreased total sleep time with more awakenings, less stage 4 sleep, decreased rapid-eye-movement (REM) efficiency, and shortened REM latency compared with those of a group of age- and sex-matched normal subjects. These abnormalities generally resembled those of an age-matched group of depressed patients, although significant differences remained. These findings suggest that such sleep abnormalities as shortened REM latency may not be entirely specific for primary affective illness. They also point to a possible biological link between OCD and affective illness.

Adult↗
PubMed1982

REM sleep suppression induced by selective monoamine oxidase inhibitors.

The effects of 4 weeks of treatment with the selective monoamine oxidase (MAO) inhibiting antidepressant clorgyline and pargyline on the sleep of affectively disordered patients were studied. Both inhibitors resulted in near total suppression of REM sleep, a decrease in total sleep time, and an increase in the percent of stage 2 sleep. Clorgyline also increased awake time and decreased total recording period and sleep latency. In general, changes were greater for clorgyline than for pargyline and were about 50% slower to return to baseline after clorgyline compared to pargyline discontinuation. The results were consistent with the hypothesis that selective inhibition of the MAO type A, as produced by clorgyline, is sufficient to induce marked sleep changes. MAO inhibitor-induced receptor changes are proposed to account for the time course of the REM suppression and the REM rebound observed upon withdrawal.

Adult↗
PubMed1982

Lifetime monoamine oxidase inhibition and sleep.

The effects of clorgyline, a type A monoamine oxidase (MAO) inhibitor, on the sleep of the rat were examined after subacute and lifetime administration. When 2 mg/kg 24 hours were given for 60 hours, type A MAO was inhibited by 92% and a significant reduction in REM sleep time was noted. When fetal rats were exposed to maternal dosage of 1 mg/kg/24 hours and then received this dose from one to 6 weeks postnatally, type A MAO was inhibited by 99%, but there were no alterations in the EEG sleep stages. In summary, subacute administration of clorgyline resulted in decreases in both Type A MAO and REM sleep; during chronic administration in a developing animal, Type A MAO was again decreased, but there was no corresponding change in REM sleep.

Animals↗