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Biomedical subjects

D B Jarrett

Publications and source records attributed to D B Jarrett.

At least 37 records · Page 2Linked to original sources
PubMed1989

Sleep EEG and DST findings in anergic bipolar depression.

The authors report sleep EEG and dexamethasone suppression test (DST) findings for a homogeneous sample of anergic bipolar depressed outpatients (bipolar I, N = 7; bipolar II, N = 19) characterized by motor retardation, volitional inhibition, hypersomnia, or weight gain and sleep EEG findings for 26 age- and sex-matched normal control subjects. Sleep architecture was abnormal in bipolar depression, particularly with respect to little stage 1 sleep. The biological profile of an anergic episode of bipolar depression did not include a shorter than normal mean REM latency, poor sleep continuity, or abnormally low amounts of stages 3 and 4 sleep, and only three (13%) of 23 patients manifested cortisol nonsuppression.

Adult↗
PubMed1989

Treatment of imipramine-resistant recurrent depression: II. An open clinical trial of lithium augmentation.

Prior studies suggest that the addition of lithium salts may enhance treatment responses in depressions that have not responded to tricyclic antidepressants. The authors report on the efficacy of lithium augmentation in an open-label study of 20 outpatients with recurrent major depression who had not responded to greater than or equal to 12 weeks of treatment with imipramine (mean dosage = 256 mg/day) and psychotherapy. Only 1 patient (5%) responded during the first week of treatment, but the cumulative response rate increased to 65% during the 6-week clinical trial. Improvement in patients receiving lithium augmentation was significantly greater than the improvement observed in a historical control group of imipramine-resistant patients who received continued treatment with the imipramine-psychotherapy combination. The results support the usefulness of a 6-week trial of lithium augmentation in outpatients with resistant depression. It remains unclear whether the effectiveness of lithium augmentation is due to a true potentiation effect, a primary antidepressant effect by lithium, or a combination of both those factors.

Adult↗
PubMed1989

Treatment of imipramine-resistant recurrent depression: I. An open clinical trial of adjunctive L-triiodothyronine.

Prior studies suggest that supplemental treatment with thyroid hormone may enhance the patient's response in depression resistant to tricyclic antidepressants. The authors report on the lack of efficacy of adjunctive L-triiodothyronine (T3; 25 micrograms/day) in a sample of 20 outpatient unipolar depressives who had not responded to greater than or equal to 12 weeks of treatment with imipramine (mean dosage = 240 mg/day) and interpersonal psychotherapy. The overall response rate after 4 weeks of T3 was low (25%); the outcome did not differ significantly from a matched historical comparison group who received continued tricyclic treatment but not T3.

Adult↗
PubMed1988

Acute changes in sleep-related hormone secretion of depressed patients following oral imipramine.

Tricyclic antidepressants have acute effects on hormone secretion when given either orally or parenterally in the morning. These drugs also have acute effects on the sleep electroencephalogram (EEG) when given immediately before sleep onset. In particular, imipramine significantly delays the REM-nREM cycle and increases the amount of delta wave activity. This study shows that an oral dose of 50 mg imipramine given at bedtime to depressed patients has little effect on the secretion of prolactin and melatonin, but acutely advances the secretion of growth hormone and cortisol. This suggests that sleep and hormone secretion may only be temporally related, as they can be dissociated pharmacologically.

Administration, Oral↗
PubMed1988

Vasopressin stimulation of adrenocorticotropin hormone (ACTH) in humans. In vivo bioassay of corticotropin-releasing factor (CRF) which provides evidence for CRF mediation of the diurnal rhythm of ACTH.

The diurnal response of ACTH release to intravenously administered arginine vasopressin was tested in normal volunteers given consecutively moderate doses of vasopressin every 15 min (0.1, 0.3, 1.0, and 3.0 IU) at 2200 h and again at 0700 h (PM/AM). This protocol was repeated 4 wk later with the times reversed (AM/PM). A dose-related increase in ACTH secretion was observed in all subjects. When the AM response of the AM/PM protocol was compared with the PM response of the PM/AM protocol, the release of ACTH was greater in the morning (P less than 0.05) as evaluated by the following criteria: peak value of ACTH (129.9 +/- 30.4 pg/ml in the AM vs. 57.1 +/- 20.2 in the PM); area under the curve (689 in the AM vs. 259 in the PM); and, sensitivity of the ACTH dose-response curve (first significant increase in ACTH with 1 IU of vasopressin in the AM but not significant even after 3 IU in the PM). In addition, when the AM vasopressin testing followed a previous evening stimulation (PM/AM protocol), there was a blunted ACTH response compared with the AM/PM protocol. Corticotropin-releasing factor (CRF) is probably the major ACTH secretagogue, but since vasopressin acts synergistically with CRF to produce an augmented release of ACTH, we suggest that the ACTH response to administered vasopressin depends upon the ambient endogenous level of CRF. We interpret our data and published data that CRF produces a lesser release of ACTH in the AM as follows: in the morning endogenous CRF is high and administered CRF produces little further release of ACTH, but administered vasopressin acting synergistically with high endogenous CRF causes a greater release of ACTH; conversely, in the evening endogenous CRF is low and administered CRF causes a greater release of ACTH, but vasopressin (a weak secretagogue by itself) gives a low ACTH response. We conclude that vasopressin stimulation of ACTH secretion can be used as an in vivo bioassay of endogenous CRF, and that there is a diurnal rhythm of CRF in hypophyseal portal blood.

Adrenocorticotropic Hormone↗
PubMed1987

Prolactin secretion during sleep: a comparison between depressed patients and healthy control subjects.

Although several neuroendocrine abnormalities have been described in depressed patients, relatively little attention has been paid to the pattern of prolactin secretion during sleep. Sleep disturbances are frequently found in depressed patients, and the sleep electroencephalogram (EEG) typically shows significant changes in the first and last 100 min, when prolactin secretion frequently occurs. In this study, carefully defined inclusion criteria were used to ensure comparability in the quality of the sleep maintenance, so that the pattern of sleep-related prolactin secretion in a group of 26 depressed inpatients could be compared to that in a group of 20 healthy control subjects. Starting from sleep onset, the patients did not show any statistically significant difference in either the serum prolactin concentration or the pattern of integrated prolactin secretion relative to the control subjects. A statistically significant relationship between prolactin secretion and the REM-non-REM sleep cycle could not be demonstrated in these subjects.

Adult↗
PubMed1987

Pregnancy-related affective episodes among women with recurrent depression.

The authors examined 52 women with recurrent depression to determine the differences between women with and without histories of pregnancy-related affective episodes. The women with histories of such episodes (N = 24) had been significantly younger at illness onset, were more severely depressed at baseline, and tended to show less emotional stability. The EEG-recorded sleep of the women with pregnancy-related affective episodes was distinguished by longer REM sleep time and more REM activity, differences accounted for almost entirely by the women with histories of only postpartum episodes.

Adult↗
PubMed1987

Identification of a corticotropin-releasing factor-binding protein in the plasma membrane of AtT-20 mouse pituitary tumor cells and its regulation by dexamethasone.

CRF stimulates the synthesis and secretion of proopiomelanocortin-derived peptides from AtT-20 mouse pituitary tumor cells. This study has shown that there is a specific binding site for CRF located on the plasma membrane of these cells. Both [125I]iodo-Tyr0CRF and noniodinated CRF (10(-11)-10(-7) M) stimulated, in a dose-dependent manner, the secretion of equimolar amounts of beta-endorphin-like immunoactivity from AtT-20 cells. Disuccinimidyl suberate, a cross-linking agent, was used to demonstrate specific binding of [125I]iodo-Tyr0CRF to plasma membranes from these cells. After cross-linking [125I] iodo-Tyr0CRF, the membrane proteins were solubilized with sodium dodecyl sulfate and electrophoresed on a 10% polyacrylamide gel. A single radioactively labeled band, corresponding to a mol wt of 66,000, was identified by autoradiography. [125I]Iodo-Tyr0CRF binding to these membranes was inhibited by 10(-7) M unlabeled CRF or an equimolar concentration of the CRF analog sauvagine. Similar concentrations (10(-7) M) of TRH, GnRH, insulin, [Arg8]vasopressin, somatostatin, and ACTH did not inhibit [125I]iodo-Tyr0CRF binding to the plasma membranes. Incubation of AtT-20 cells for 24 h in the presence of 10 nM dexamethasone reduced [125I]iodo-Tyr0CRF binding by 80% compared to that in untreated cells. Dexamethasone also inhibited the CRF-stimulated beta-endorphin-like immunoactivity secretory response. These data indicate that binding of CRF to a specific membrane protein is an integral component in the stimulation of AtT-20 cells by CRF.

Animals↗
PubMed1985

Electroencephalographic sleep of younger depressives. Comparison with normals.

The electroencephalographic sleep of younger depressives (aged 20 to 44 years) was compared with that of an age-matched group of normals. The patients demonstrated many of the typical sleep changes reported for older depressed populations: shortened rapid-eye-movement (REM) latency; REM sleep activity alterations, with a shift to the early portion of the night (first REM period); reduced delta sleep; and sleep efficiency reductions marked by sleep-onset difficulties. The traditional scoring procedures were supplemented by automated REM and delta-sleep analyses that provided more precise delineation of these differences between patients and normals, particularly the distributions of REM activity and delta-wave patterning.

Adult↗
PubMed1985

Effect of benztropine on the diurnal prolactin responses to haloperidol.

Prolactin (PRL) responses to haloperidol were investigated at 0900 and 1800 h in six young healthy men under basal conditions and after benztropine mesylate administration. Haloperidol administration induced significantly higher PRL release during the evening compared to the morning. The anticholinergic drug, benztropine, potentiated the PRL responses to haloperidol both in the morning and in the evening. The possible mechanisms of these findings are discussed.

Adult↗
PubMed1985

Biosynthesized [35S]methionine-labeled pro-opiomelanocortin peptides as novel recovery markers in radioimmunoassay of peptide hormones.

Hormones are extracted from plasma with varying efficiency. Thus, markers or internal standards are often needed, to monitor and correct for extraction losses. To do so is difficult in the case of peptide hormones because radioactive recovery markers either have a low specific activity or, if labeled with iodine, may not be fully representative because of alterations in their size and charge. More importantly, markers labeled with 125I can interact in, and thus compromise, the subsequent radioimmunoassay. AtT-20 mouse pituitary tumor cells, which can be stimulated to synthesize and secrete pro-opiomelanocortin peptides, can biosynthetically label beta-lipotropin (beta-LPH) with [35S]methionine. The labeled peptide, which is co-eluted with unlabeled beta-LPH in "high-performance" liquid chromatography, is fully immunoprecipitable and has a specific activity of 34 Ci/g. We use this labeled peptide to monitor the recovery of beta-LPH in silicic acid extraction from plasma. This peptide is an ideal marker of analytical recovery because it does not interfere in subsequent radioimmunoassays.

Animals↗
PubMed1984

Attrition in maintenance therapy for recurrent depression. A preliminary report.

All maintenance treatment programs are complicated by the issue of patient noncompliance. This report investigates factors contributing to noncompliance during a 2-year study designed to evaluate the efficacy of long-term antidepressant medication in patients with recurrent unipolar depression. Only 21 of 51 patients (49%) who entered maintenance treatment successfully completed this phase of the study. Fifteen patients (8 completers and 7 dropouts) were randomly selected for an interview which focused on their previous psychiatric treatment history and attitudes towards the maintenance treatment program. In addition, these patients also completed a comprehensive personality battery. Results indicate that, while both groups had similar attitudes about the treatment program, they differed significantly along personality and psychiatric treatment history variables. Dropouts scored higher than completers on a measure of hysterical personality style. They were also more likely to have received psychotherapy in previous treatment experiences and to rate it as beneficial, while completers consistently rated prior treatment, which did not include antidepressant medication, as being of no benefit whatsoever. In order to enhance patient compliance, it is important to obtain information early in treatment about patients' treatment histories and their expectations about effective treatment for depression.

Adult↗
PubMed1984

The effects of dexamethasone administration on EEG sleep in depressed patients.

Since DST non-suppression and sleep abnormalities have been shown to co-exist in depressive states, it seems important to examine what effects dexamethasone administration might have on the sleep of depressed patients. Therefore, the effects of 1 mg dexamethasone p.o. administered at 11 p.m. to a group of 12 depressed outpatients was examined. In this series of patients, the hypothesis of no significant changes in sleep continuity, sleep architecture or REM sleep features was confirmed aside from an increase in Stage 2 sleep percent and decrease in Stage 1 REM percent in these patients (both variables stayed in the normal range). It can be concluded that acute administration of dexamethasone does not influence the sleep of depressed patients in a major way.

Adult↗
PubMed1984

Biological and clinical predictors of response in recurrent depression: a preliminary report.

Electroencephalographic (EEG) sleep and selected hormone measurements were investigated in a group of 34 recurrent depressives receiving both pharmacotherapy and psychotherapy. These biological variables were examined to determine whether such measures could predict the rapidity of treatment response. While the EEG measures of sleep onset difficulty and degree of rapid eye movement (REM) density provided some level of discrimination, the serum cortisol measure, particularly the cortisol nadir, significantly discriminated between normal responders and slow or nonresponders. These data support the notion that biological factors measured before treatment might relate to the rapidity and extent of clinical response achieved by the patient.

Adult↗
PubMed1984

Application of automated REM and slow wave sleep analysis: I. Normal and depressed subjects.

Computerized analysis of rapid eye movement (REM) and delta electroencephalographic (EEG) sleep patterns in normal and depressed subjects offers opportunities to examine sleep more precisely than previously possible. In the present study, automated REM analyses demonstrated good reliability with traditional manual procedures in both normal and depressed subjects. However, automated delta analyses correlated well with traditional scoring in normal subjects, but not in depressed patients. These findings suggest the use of automated delta techniques similar to those employed in this report or spectral analytic techniques in the following types of studies: specificity of delta sleep in various psychiatric syndromes, changes in delta sleep produced by the administration of psychotropic agents, relationships between delta sleep and sleep-related neuro-endocrine patterns, and, finally, relationships between delta sleep patterns and other biological rhythms such as activity and temperature.

Adult↗
PubMed1984

Application of automated REM and slow wave sleep analysis: II. Testing the assumptions of the two-process model of sleep regulation in normal and depressed subjects.

Abnormalities in a two-process model of sleep regulation (a sleep-dependent process, termed Process S, and a sleep-independent circadian process, termed Process C) have been proposed to account for sleep abnormalities in depressive states. The major tenets of the two-process model of sleep regulation as applied to depression are: the level of process S, as reflected by the electroencephalographic (EEG) slow-wave activity, corresponds to the sleep-dependent facet of sleep propensity; the pathognomonic changes of sleep in depressives are a consequence of a deficiency in the build-up of process S. The application of automated rapid eye movement (REM) and delta wave analyses in normal subjects and younger depressed patients supports the model to some extent: The time spent asleep is positively correlated with total delta waves (normals and depressives) and average delta waves (depressives); delta sleep is lower in depressives than in normals; the average delta wave count is significantly reduced in younger depressives over the total night and in non-REM period 1. The model also postulates that measures of phasic REM activity are inversely related to process S, suggesting that process S can be regarded as exerting an inhibitory influence on phasic REM activity.

Adult↗