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Biomedical subjects

J C Gillin

Publications and source records attributed to J C Gillin.

At least 163 records · Page 9Linked to original sources
PubMed1987

Low natural killer cytotoxicity in major depression.

Natural killer cell cytotoxicity was significantly lower in a group of hospitalized depressed men than in matched controls. The absolute number of neutrophils was increased in the depressed group, but the numbers of other cell types did not differ between groups. These findings further demonstrate that altered immunity is a biologic concomitant of affective disorders.

Cytotoxicity, Immunologic↗
PubMed1987

Relation of pontine choline acetyltransferase immunoreactive neurons with cells which increase discharge during REM sleep.

The purpose of this study was to determine whether neurons in the medial pontine reticular formation with high discharge rates during REM sleep could be localized in regions of the brainstem having neurons displaying choline acetyltransferase immunoreactivity. Six cats were implanted with sleep recording electrodes and microwires to record extracellular potentials of neurons in the pontine reticular formation. Single-units with a S:N ratio greater than 2:1 were recorded for at least two REM sleep cycles. A total of 49 units was recorded from the pontine reticular formation at medial-lateral planes ranging from 0.8 to 3.7 mm. The greatest proportion of the units (28.6%) showed highest discharge during active waking and phasic REM sleep compared to quiet waking, non-REM sleep, transition into REM sleep or quiet REM sleep periods. A percentage (20.4%) of the cells had high discharge associated with phasic REM sleep periods while 8.2% of the cells showed a progressive increase in discharge from waking to REM sleep. Subsequent examination of the distribution of choline acetyltransferase immunoreactive cells in the PRF revealed that cells showing high discharge during REM sleep were not localized near presumed cholinergic neurons. Indeed, we did not find any ChAT immunoreactive somata in the medial PRF, an area which has traditionally been implicated in the generation of REM sleep. These results suggest that while increased discharge of PRF cells may be instrumental to REM sleep generation, these cells are not cholinergic.

Animals↗
PubMed1987

Cardiovascular, catecholamine and psychological responses to TRH in four types of affective disorder patients.

When 500 micrograms of TRH is given intravenously, an increase in TSH, blood pressure, plasma catecholamines and positive emotions follows. Four groups of patients with major, minor or bipolar depression or schizoaffective disorder increased their TSH levels by similar amounts after TRH. The neurohormone also significantly increased diastolic blood pressure by 5.5 +/- 1.6 mm Hg, and decreased heart rate by 7.6 +/- 1.3 beats/min. There was a weak trend for bipolar depressives to have less cardiovascular response to TRH than the other groups. Plasma norepinephrine (NE) was higher after TRH than after placebo. The NE response differed between patient groups (P = .0023) because of a smaller response by major depressives. TRH decreased anger, tension and depression, and increased friendliness. Positive emotional responses were significantly greater in the bipolar depressives than in other groups. Forty-one other studies have found a subnormal TSH response does not distinguish between subtypes of the affective disorders, but cardiovascular, catecholamine and mood responses may do so.

Adult↗
PubMed1987

Measurement of ACTH and prolactin in the dexamethasone suppression test.

Plasma concentrations of ACTH and prolactin were measured in psychiatric inpatients at 8 a.m. and 4 p.m. before and after the standard 1 mg overnight Dexamethasone Suppression Test (DST). Plasma concentrations of cortisol were measured at 8 a.m. and 4 p.m., and 11 p.m. before and after 1 mg dexamethasone. Dexamethasone suppressed plasma concentrations of ACTH, prolactin and cortisol in the subject group as a whole. "Cut Points" obtained using Fisher's Exact Test identified plasma ACTH values at 8 a.m. baseline, 4 p.m. baseline and 8 a.m. post-dexamethasone and plasma prolactin values at all four times that significantly differentiated patients with bipolar depressive disorder and major depressive disorder from other psychiatric patients. There were no cut points found at any of the six times for plasma levels of cortisol that significantly differentiated between these two diagnostic groups. Of interest in this subject population, basal (pre-dexamethasone) plasma concentrations were of more diagnostic information than post-dexamethasone values. These pilot findings suggest that monitoring plasma prolactin and ACTH concentrations before and after dexamethasone might increase the sensitivity and specificity of this laboratory test for depression.

Adrenocorticotropic Hormone↗
PubMed1987

Depressing normal sleep: two tests of the Process S deficiency hypothesis.

It has been hypothesized that sleep changes in endogenous depression are caused by a deficiency in the buildup of Process S (a sleep/wake-dependent component of sleep thought to be reflected in EEG power), and a resulting disinhibition of the REM sleep system. To test this hypothesis, we have reexamined the results of two studies in which sleep episodes of normal subjects could be considered to be similarly deficient in Process S, as a result of reduced prior wakefulness. Structural components of these sleep episodes, particularly REM sleep measures, showed remarkable similarities to those observed in depressed patients. Moreover, there was a strong relationship between REM latency and preceding slow-wave sleep. The findings are interpreted as providing support for the Process S deficiency hypothesis.

Adolescent↗
PubMed1987

Pulsatile rhythms of adrenocorticotropin (ACTH) and cortisol in women with endogenous depression: evidence for increased ACTH pulse frequency.

Plasma ACTH and serum cortisol levels were measured at 20-min intervals for 24 h in six young women with unipolar endogenous depression and in eight normal women during the early follicular phase of the menstrual cycle. The women with depression had a marked increase (P less than 0.005) in mean ACTH pulse frequency [14.5 +/- 0.6 (+/-SE) pulses/24 h] compared with normal women (9.9 +/- 0.7 pulses/24 h), while mean ACTH pulse amplitude and 24-h transverse mean ACTH levels were similar in the two groups. In contrast, 24-h transverse mean cortisol levels were higher (P less than 0.02) in the depressed women (242 +/- 28 nmol/L) than in the normal women (163 +/- 10 nmol/L). This hypercortisolemia in the depressed women was accompanied by markedly increased (P less than 0.001) episodic cortisol secretion (286 +/- 24 X 10(2) nmol/L X min) compared with that in normal women (155 +/- 17 X 10(2) nmol/L X min), and the secretory episodes were both longer in duration (P less than 0.05) and of higher amplitude (P less than 0.05) in the depressed women. The circadian variations in ACTH and cortisol were maintained in these depressed women, and the times of the circadian nadir, as determined by cosinor analysis, were similar to those in the normal women. However, the mean length of the evening quiescent period of cortisol secretion was far shorter (P less than 0.005) in the depressed women (27 +/- 8 vs. 202 +/- 40 min). Moreover, the postlunch rise in serum cortisol was significantly higher (P less than 0.02) in the depressed women (204 +/- 29 vs. 111 +/- 15 nmol/L). These results provide evidence that the hypercortisolism in depressed women is associated with an increase in ACTH pulse frequency, expanded cortisol secretory episodes, including a greater postlunch rise in cortisol, and a shortened evening quiescent period of cortisol secretion. Our findings provide evidence for centrally mediated activation of the ACTH-cortisol system in women with depression without a phase shift in circadian rhythm.

Adrenocorticotropic Hormone↗
PubMed1986

Rapid-eye movement sleep and muscarinic receptor binding in rats are augmented during withdrawal from chronic scopolamine treatment.

The purpose of this study was to determine whether a seven day, once-daily morning administration of scopolamine produces upregulation of muscarinic receptors and augments REMS during withdrawal. After obtaining two, six-hour baseline sleep recordings, beginning at 0900, independent groups of rats were administered either scopolamine or saline every morning for seven days. Six hour sleep recordings were obtained following the first and seventh day of injection and during the two subsequent withdrawal days. After obtaining the last sleep recording the rats were sacrificed and the following brain areas removed: cerebral cortex, hippocampii, caudate nuclei, brainstem, and cerebellum. 3H-QNB was used as the ligand to assess for changes in muscarinic receptor binding. Compared to baseline, scopolamine produced a significant decrease in REMS during the period of drug administration. During the withdrawal days, however, REMS increased during the morning period. Compared to the saline group, the scopolamine treated animals had increased muscarinic receptor binding in the caudate and hippocampus; no significant change in receptor density was observed in the cortex, brainstem or cerebellum.

Animals↗
PubMed1986

Specific [3H]-N-methyl scopolamine binding without cholinergic function in cultured adult skin fibroblasts.

Cultured adult skin fibroblasts were studied for binding and functional evidence of muscarinic receptors in order to assess their utility as a model of cholinergic function in affective illness. Saturable, specific, high affinity binding could be demonstrated in intact cells from some cell lines with [3H]-NMS, but not [3H]-QNB, presumably because of intracellular trapping of unbound [3H]-QNB. [3H]-NMS specific binding indicated a single site with a KD of approximately 210 pM. [3H]-NMS was displaced by cholinergic agonists and antagonists with relative affinities similar to muscarinic receptors in brain. Many cell lines, however, showed no specific binding. No functional response to carbachol could be demonstrated with respect to inhibition of isoproterenol-stimulated cyclic AMP formation, stimulation of cyclic GMP formation or stimulation of phosphoinositide hydrolysis in any cell line regardless of either high or no specific [3H]-NMS binding.

Adult↗
PubMed1986

Stress-induced immobility in rats with cholinergic supersensitivity.

Immobility during forced swimming or after mild footshock (1 mA for 2 sec) was observed in five groups of rats. The Flinders Sensitive Line (FSL) of rats, known to be more sensitive to cholinergic agonists, exhibited the greatest degree of immobility in the forced swim test. Rats chronically treated with, and subsequently withdrawn from, either scopolamine (2 mg/kg, once daily) or amitriptyline (10 mg/kg, once daily) were also significantly more immobile than either a control group treated chronically with isotonic saline or the Flinders Resistant Line (FRL) of rats in the forced swim test. Similar trends were observed for locomotor depression in the open field following exposure to footshock. Receptor binding studies indicated significantly greater concentrations of muscarinic acetylcholine receptors in the hippocampus of the scopolamine, and amitriptyline, withdrawn rats. These findings indicate that rats with increased cholinergic sensitivity are more sensitive to the immobility-inducing effects of mild stressors. Thus, they may prove to be useful models for studying the relationship between affective disorders and the cholinergic system.

Amitriptyline↗
PubMed1986

Central and peripheral cholinesterase inhibition: effects on anterior pituitary and sympathomimetic function.

Ten physically healthy inpatients of mixed diagnosis received, in a randomized, counterbalanced double-blind paradigm, physostigmine (22 micrograms/kg) and neostigmine (11 micrograms/kg). Infusions were separated by at least 2 days. The differential effects of physostigmine and neostigmine on plasma concentrations of cortisol, prolactin, growth hormone, ACTH, beta-endorphin/beta-lipotropin-like immunoreactivity, dopamine, norepinephrine, and epinephrine are reported. Administration of physostigmine, unlike that of neostigmine, was associated with statistically significant increases in plasma concentrations of cortisol, prolactin, ACTH, beta-endorphin/beta-lipotropin-like immunoreactivity, and epinephrine, presumably via central mechanisms. In a separate study, 15 subjects, mostly depressed inpatients, were pretreated with methscopolamine (0.75 mg) on one day and scopolamine (0.5 mg) on another day, at least 2 days apart, in a randomized, counterbalanced double blind paradigm and subsequently on each day received physostigmine (22 micrograms/kg). Scopolamine significantly attenuated the physostigmine-associated increase in plasma concentrations of cortisol, growth hormone, prolactin, ACTH, and dopamine compared to methscopolamine, and a close-to-significant attenuation of epinephrine as well. These results provide further evidence that physostigmine's effects on plasma concentrations of pituitary hormones and epinephrine occur via central mechanisms and are muscarinically mediated.

Adrenocorticotropic Hormone↗