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Biomedical subjects

J C Gillin

Publications and source records attributed to J C Gillin.

At least 127 records · Page 7Linked to original sources
PubMed1990

Pilocarpine, an orally active muscarinic cholinergic agonist, induces REM sleep and reduces delta sleep in normal volunteers.

The effect of oral pilocarpine, a direct-acting muscarinic, cholinergic agonist, on polygraphic sleep parameters was studied in 13 healthy male volunteers. Subjects received placebo and oral pilocarpine (25 mg) in a double-blind, counterbalanced, crossover design. Pilocarpine shortened the latency of rapid eye movement (REM) sleep and increased total REM time, REM%, and the duration of the first REM period. In addition, it reduced Stage 4 sleep and Delta sleep. Pulse rate was not significantly changed during the first hour of darkness after administration of pilocarpine. Subjective sleep experience and the subjects' condition in the morning were not altered. These results suggest that pilocarpine has central effects (i.e., induction of REM sleep) that are similar to those of other centrally acting muscarinic cholinomimetic agents.

Administration, Oral↗
PubMed1990

Melatonin suppression in bipolar and unipolar mood disorders.

Nocturnal melatonin suppression to 500 lux light was studied during an acute episode of illness in 8 patients with bipolar disorder, 7 patients with unipolar depression, and 15 age-, sex-, and season-matched normal controls. Unipolar patients did not differ from controls in melatonin suppression. In contrast to previous studies, controls showed greater melatonin suppression than bipolar patients. Baseline melatonin concentration, however, was significantly lower in the bipolar group compared to the unipolar and control groups.

Bipolar Disorder↗
PubMed1990

Short REM latency in primary alcoholic patients with secondary depression.

Primary alcoholic patients with secondary depression had significantly shorter REM latency and less non-REM sleep than alcoholics without other psychiatric diagnoses and normal control subjects. Both patient groups had significantly longer sleep latency and less sleep efficiency, total sleep time, and delta sleep than control subjects.

Adult↗
PubMed1990

Differential effects of cholinergic antagonists on REM sleep components.

We examined the effects of cholinergic receptor blockers on changes in rapid eye movement (REM) sleep components. M1 and M2 muscarinic receptor antagonists or atropine were microinfused before an M2 muscarinic receptor agonist, and the effects on individual REM sleep components were assessed. All drugs were microinjected into the same locus within the medial pontine reticular formation in cats, and sleep recordings were made for at least 3 hours postinjection. Results suggest that desynchronized electroencephalogram (EEG) is influenced by the M1 muscarinic receptor, muscle atonia is influenced by the M2 muscarinic receptor, and ponto-geniculo-occipital (PGO) waves are affected by the nicotinic receptor.

Animals↗
PubMed1989

Effect of specific M1, M2 muscarinic receptor agonists on REM sleep generation.

Specific agonists for muscarinic receptor subtypes were infused by microinjection into the medial pontine reticular formation of freely moving cats. The M2 agonists Oxotremorine-M and Cisdioxolane significantly increased REM sleep percentage. The results obtained with microinfusions of carbachol, a mixed muscarinic agonist, were similar to that obtained by the M2 agonists. The M1 agonist McN-A-343 did not elicit any change in sleep or REM sleep percentage. The generation of REM sleep by cholinergic stimulation of the medial pontine reticular formation may be mediated by the M2 muscarinic receptor subtype.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1989

Mitogen-stimulated lymphocyte proliferation and pituitary hormones in major depression.

To assess cellular immune status and the hypothalamic-pituitary (HP) axis in patients with major depression, we examined peripheral blood mononuclear cells (PBMC) and measured the plasma levels of cortisol, adrenocorticotropin hormone (ACTH), growth hormone (GH), and prolactin (PRL). Twenty patients with major depression were compared with 20 control subjects matched for age, sex, and race. The dose-response curves for concanavalin-A (Con-A) and phytohemagglutinin (PHA) stimulation were not significantly different between the two groups. The patients had decreased Con-A-stimulated T-lymphocyte proliferation when compared to the control subjects, but only at the lowest suboptimal concentration of Con-A. None of the four concentrations of PHA-stimulated proliferation were different between the two groups, neither was PHA-induced interleukin-2 production. Within the patient group only, plasma prolactin (PRL) correlated significantly with stimulated lymphocyte proliferation using two optimal concentrations of PHA and one optimal concentration of Con-A, when the proliferation was expressed using the stimulation index.

Adrenocorticotropic Hormone↗
PubMed1989

Neuroendocrine effects of ovine corticotropin-releasing hormone in panic disorder patients.

A number of neuroendocrine abnormalities have been reported in panic disorder patients: the most extensively studied being disturbances of hypothalamic-pituitary-adrenal function (Curtis et al. 1982; Leiberman et al. 1983; Uhde et al. 1988). The recent sequencing and synthesis of corticotropin-releasing hormone now allows direct testing of pituitary responsivity to this neuropeptide in affective and panic disorder patients (Holsboer et al. 1984; Gold et al. 1986; Roy-Byrne et al. 1986; Holsboer et al. 1987; Risch et al. 1988). We report the effects of intravenously administered ovine corticotropin-releasing hormone (0.03 micrograms/kg) on plasma concentrations of adrenocorticotropin hormone (ACTH) and cortisol in a small group of panic disorder patients and age- and sex-matched normal controls.

Adrenocorticotropic Hormone↗
PubMed1989

Regional cerebral glucose metabolic rate in human sleep assessed by positron emission tomography.

The cerebral metabolic rate of glucose was measured during nighttime sleep in 36 normal volunteers using positron emission tomography and fluorine-18-labeled 2-deoxyglucose (FDG). In comparison to waking controls, subjects given FDG during non-rapid eye movement (NREM) sleep (primarily stages 2 and 3) showed about a 23% reduction in metabolic rate across the entire brain. This decrease was greater for the frontal than temporal or occipital lobes, and greater for basal ganglia and thalamus than cortex. Subjects in rapid eye movement (REM) sleep tended to have higher cortical metabolic rates than waking subjects. The cingulate gyrus was the only cortical structure to show a significant increase in glucose metabolic rate in REM sleep in comparison to waking. The basal ganglia were relatively more active on the right in REM sleep and symmetrical in NREM sleep.

Brain↗
PubMed1989

Lithium delays circadian phase of temperature and REM sleep in a bipolar depressive: a case report.

The effects of lithium on the circadian rhythms of body temperature and rapid eye movement (REM) sleep were examined in a patient with bipolar depression. The acrophase of body temperature showed a phase delay of 74 min after 1 week of lithium treatment. REM latency increased significantly with lithium, and the onset of subsequent REM periods was also delayed. The proportion of the night spent in REM sleep decreased significantly. There was no effect of lithium on the patient's mood. The data are consistent with the hypothesized phase-delaying properties of lithium but do not support the causal link between circadian phase and affective state.

Bipolar Disorder↗
PubMed1989

Effects of brief naps on mood and sleep in sleep-deprived depressed patients.

To determine the effects of brief naps on mood and electroencephalographic (EEG) sleep in sleep-deprived depressed patients, data from 19 hospitalized patients with depression were analyzed; all were kept awake from 0700h until the following day, when they were allowed 10-min naps at either 0830h or 1500h. Six of the patients showed a clinically significant improvement (greater than 40% change) on the Hamilton Rating Scale for Depression (HRSD) before the nap after all-night sleep deprivation, and the group as a whole showed a significant improvement on the HRSD, the Profile of Mood States, and the Brief Psychiatric Rating Scale subscale for depression. Naps did not alter mood in the responders, but did improve measured depression on the HRSD in the non-responders. Morning and afternoon naps did not differ significantly in their effects on mood or nap sleep. On the recovery sleep, patients who were classified as responders after the nap showed a significantly greater increase in delta (Stage 3 + 4) sleep compared with baseline than nonresponders.

Affect↗
PubMed1989

Light suppression of melatonin in unipolar depressed patients.

The effects of nocturnal light (500 lux) exposure on plasma melatonin were studied in seven men suffering from unipolar depression and in seven healthy men. Both groups showed significant declines in plasma melatonin concentrations during 1 hour's light exposure. Differential group declines were not detected.

Adult↗
PubMed1989

Biological effect of bright light.

1. Five minute bright light exposures reduced plasma levels of melatonin in eight normal subjects. 2. No significant change in ACTH levels occurred. 3. These results raise the possibility that short intense light exposures can synchronize circadian rhythms as well as benefit patients with seasonal affective disorder. They also indicate that short pulses of bright light do not affect pituitary ACTH production.

Adrenocorticotropic Hormone↗
PubMed1989

Bright light can delay human temperature rhythm independent of sleep.

New evidence suggest that the phase of human circadian (approximately 24 h) rhythms can be reset by exposures to bright artificial light. This study explored the value of 5 h of bright 3,800-6,000 lx light in resetting human circadian rhythm phases among healthy volunteers. Nine subjects were exposed to 3-5 h bright light for three evenings and to control dim light for an equivalent time, in counterbalanced orders. Electroencephalogram sleep recordings, overnight rectal temperature measurements, and mood scales were obtained. Compared with control dim light, bright light delayed the body temperature rhythm approximately 3 h; however, sleep latency was delayed only 9 min. This suggests that bright light shifted the phase of the human circadian temperature rhythm independent of its effects on sleep phase. Resetting rhythms with bright light may prove useful in treatment of psychiatric disorders.

Adolescent↗
PubMed1989

Blunted growth hormone response to peripheral infusion of human growth hormone-releasing factor in patients with panic disorder.

Patients with panic disorder (N = 11) and age- and sex-matched normal control subjects (N = 11) were challenged with human growth hormone-releasing factor (GH-RF) (1 microgram/kg i.v.) or placebo in random order. The control subjects had significantly increased plasma growth hormone (GH) levels after GH-RF infusion whereas panic disorder patients did not. At 15 and 30 minutes after GH-RF infusion, GH concentrations were significantly higher in the control subjects than in the patients. These findings with GH-RF extend findings from earlier reports that patients with panic disorder show blunted GH response to phobic stimulation and clonidine.

Adult↗