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Biomedical subjects

D C Jimerson

Publications and source records attributed to D C Jimerson.

At least 73 records · Page 4Linked to original sources
PubMed1986

Pre-menopausal and post-menopausal depressed women.

In a consecutive series of 28 depressed women, pre-menopausal (n = 13) and post-menopausal (n = 15) patients were compared. Post-menopausal women had significantly higher levels of plasma norepinephrine, plasma 3-methoxy-4-hydroxyphenylglycol, post-dexamethasone plasma cortisol, cerebrospinal fluid 3-methoxy-4-hydroxyphenylglycol and corticotropin-releasing hormone. However, when biologic measures were adjusted for age by analyses of covariance there were no significant differences. Pre-menopausal women had had significantly more life events before the onset of depression than post-menopausal women. The implications of these findings are discussed.

Adult↗
PubMed1985

Catecholaminergic activity of the baroreceptor areas of the brain in response to bilateral dorsolateral transection of medulla oblongata in rats.

Central catecholaminergic activity was studied by measurement of norepinephrine (NE), epinephrine (EPI), their metabolites: total 3-methoxy-4-hydroxyphenylglycol (MHPG) and 3,4-dihydroxyphenylglycol in brain nuclei in response to bilateral dorsomedullary knife-cut (DMK-cut) in rats. In saline-pretreated conscious rats DMK-cut caused a marked hypertension, tachycardia and increases in plasma NE, EPI and vasopressin. Chlorisondamine (CHL) prevented the rise in plasma catecholamines and the tachycardia but failed to prevent the hypertension and the increment in plasma vasopressin. DMK-cut decreased NE and EPI in the nucleus tractus solitari (NTS) and A2 area; there were no catecholamine changes in A1 area or the periventricular nucleus but an increase in the paraventricular nucleus (PVN), the latter effect reversed by CHL. CHL alone or combined with DMK-cut had no effect on catecholamine concentrations in NTS-A2 area but lowered MHPG content. It is suggested that DMK-cut decreases the activity of the catecholaminergic system originating in A1 and terminating in PVN, where it causes catecholamine accumulation and may be involved in vasopressin release and thereby contribute to hypertension. In NTS-A2 area, however, the DMK-cut appears to increase catecholaminergic activity since catecholamines are depleted. Central effects of DMK-cut differ from those of ganglionic blockade-induced inhibition of the baroflex presumably due to sectioning of other pathways in addition to the primary baroreceptor input.

Animals↗
PubMed1985

Tyramine pressor sensitivity changes during deprenyl treatment.

Deprenyl has previously been reported to be a selective monoamine oxidase (MAO) type B inhibitor, which is associated with little or no enhancement of the pressor effects of tyramine. Employing an intravenous steady-state tyramine infusion technique, the effects of different doses of deprenyl and, for comparison, the mixed inhibitor tranylcypromine on the pressor response to tyramine were studied in 11 depressed patients. After 3 weeks of treatment, deprenyl produced dose-proportionate increases in tyramine sensitivity at all three doses (10, 30, and 60 mg/day) when compared to placebo baseline tyramine responses. While only a modest (3.7-fold) increase in tyramine sensitivity was found with the 10 mg/day deprenyl dose, the increase in tyramine sensitivity at the 60 mg/day dose of deprenyl (22-fold) approached that found with tranylcypromine. Reductions in plasma 3-methoxy,4-hydroxyphenylglycol (MHPG), used as a possible index of in vivo MAO-A inhibition, were highly correlated with increases in tyramine pressor sensitivity (r = 0.82). The data suggest that deprenyl acts as a relatively selective MAO-B inhibitor at low doses, but that this selectivity is lost at higher doses, resulting in a significant "crossover" inhibition of MAO-A and increased tyramine pressor sensitivity.

Blood Pressure↗
PubMed1985

Effects of carbamazepine on noradrenergic mechanisms in affectively ill patients.

Noradrenergic mechanisms have been postulated to account for the anticonvulsant and psychotropic effects of carbamazepine. In order to assess this possibility in man, cerebrospinal fluid (CSF) was obtained from affectively ill patients before and during treatment with carbamazepine (average duration 29 days) at doses averaging 860 mg/day, achieving blood levels of 8.86 micrograms/ml. Neither plasma nor CSF norepinephrine (NE) nor CSF 3-methoxy-4-hydroxy-phenylglycol (MHPG) was significantly altered by carbamazepine. Baseline medication-free values in 21 depressed patients were not predictive of the degree of subsequent clinical antidepressant response. CSF NE decreased in four manic patients treated with carbamazepine. The many effects of carbamazepine on noradrenergic mechanisms in animals are discussed in relationship to these first studies of carbamazepine in man.

Affective Disorders, Psychotic↗
PubMed1985

Altered norepinephrine metabolism following long-term weight recovery in patients with anorexia nervosa.

This study evaluated the relationship between noradrenergic function and long-term weight recovery in patients with anorexia nervosa. Eleven patients with long-term weight maintenance (6 to 72 months) had lower plasma and cerebrospinal fluid concentrations of norepinephrine and 3-methoxy-4-hydroxy-phenylglycol than did healthy controls. Reduced noradrenergic activity may be associated with long-term stability of weight recovery in patients with anorexia nervosa.

Adolescent↗
PubMed1985

Biological alterations in the primary affective disorders and other tricyclic-responsive disorders.

Noradrenergic function was studied in patients with primary affective disorder and other tricyclic-responsive disorders including obsessive-compulsive disorder, anorexia nervosa and panic attack/agoraphobia in medication-free states. Pre-synaptic noradrenergic activity was assessed by assaying plasma concentrations of norepinephrine (NE) and its metabolite 3-methoxy,4-hydroxyphenylglycol (MHPG). Noradrenergic receptor responsiveness was evaluated by measuring plasma growth hormone (GH), MHPG, and NE responses to clonidine. Binding of tritiated dihydroergocriptine (3H-DHE) and biochemical responsiveness of alpha 2-adrenergic receptors were measured in platelet preparations. These studies suggest that noradrenergic activity may be altered in several tricyclic-responsive disorders and are consistent with the possibility that tricyclic antidepressants may serve to stabilize a dysregulated noradrenergic system in patients from several diagnostic categories.

Adult↗
PubMed1984

The effect of desmethylimipramine on the metabolism of norepinephrine.

Eleven normal volunteers were given an acute and two chronic doses of desipramine (DMI). The plasma norepinephrine (NE), 3-methoxy-4-hydroxyphenylglycol (MHPG), and dihydroxyphenylglycol (DHPG) concentrations were measured before and during drug administration. DMI reduced plasma concentrations of MHPG by 13% and DHPG by 17%. After two weeks of drug administration, the MHPG/NE ratio was reduced, and there was a significant negative correlation with the concurrent drug concentration. These results suggest that DMI: (1) reduces the turnover of NE; and (2) diminishes the oxidative deamination of NE. In addition, the drug concentration response relationship indicates that the effects of uptake inhibition may not be maximal until concentrations in the apparent therapeutic range are achieved.

Adult↗
PubMed1984

Plasma cortisol and catecholamine responses to intracerebroventricular administration of CRF to rhesus monkeys.

Synthetic ovine corticotropin releasing factor (CRF) was administered directly into the 4th ventricle of rhesus monkeys. A dose dependent increase in plasma cortisol was observed following 10 micrograms/kg, 20 micrograms/kg, and 60 micrograms/kg of CRF. Increases in plasma epinephrine were also evident following the highest dose of CRF. Plasma norepinephrine, mean arterial pressure, and heart rate did not increase significantly following CRF administration. These data suggest that in the rhesus monkey, central administration of ovine CRF leads to activation of the pituitary-adrenocortical axis at doses that do not raise plasma catecholamines.

Animals↗
PubMed1984

Plasma cortisol responses to clonidine in depressed patients and controls. Evidence for a possible alteration in noradrenergic-neuroendocrine relationships.

Plasma cortisol responses to the intravenous administration of clonidine hydrochloride and placebo were evaluated in depressed patients and controls. Depressed patients had higher mean baseline cortisol levels than controls. Cortisol levels decreased during the morning study period following both placebo and 2 micrograms/kg of clonidine hydrochloride in the depressed patients, but the cortisol decrease was sixfold greater on the day of clonidine administration; these placebo-clonidine differences were statistically significant, whether calculated on an absolute decrement basis or as a percent change. In contrast, controls responded to clonidine with only a 1.5-fold greater cortisol reduction than that found after placebo, a nonsignificant difference from the day of placebo administration. Reductions in the concentration of plasma 3-methoxy-4-hydroxyphenylglycol following clonidine administration were significantly negatively correlated with baseline plasma cortisol levels, raising the possibility that abnormalities in the responsiveness of the alpha 2-noradrenergic system may be associated with the hypothalamo-pituitary-adrenal (HPA) axis dysfunction found in depressed patients.

Aged↗
PubMed1984

Norepinephrine and MHPG levels in CSF and plasma in Alzheimer's disease.

Postmortem findings of decreased brain norepinephrine (NE) content and decreased locus ceruleus neuronal density have suggested a possible noradrenergic deficit in Alzheimer's disease (AD). We assessed CNS and peripheral noradrenergic function in patients with advanced AD, moderate AD, and age-matched normals by measuring NE and the NE metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) levels in CSF and plasma. Subjects were drug free for at least two weeks. Plasma and CSF NE and MHPG levels were significantly higher in patients with advanced AD than in either patients with moderate AD or normal controls, while values in the patients with moderate AD did not differ from those in normal controls. These findings do not support either a central or peripheral noradrenergic deficit in AD. Rather, they suggest increased CNS and peripheral noradrenergic activity in advanced stages of the disease.

Aged↗
PubMed1984

A benzodiazepine receptor-mediated model of anxiety. Studies in nonhuman primates and clinical implications.

beta-Carboline-3-carboxylic acid ethyl ester (beta-CCE) binds with high affinity to brain benzodiazepine receptors and has potent behavioral and physiologic effects in primates. Dose-related increases in behavioral agitation, plasma cortisol level, BP, and heart rate were observed after administration of doses between 50 and 500 micrograms/kg of beta-CCE to rhesus monkeys. All of these effects were blocked by pretreatment with diazepam. Pretreatment with clonidine hydrochloride and propranolol hydrochloride, both of which have been reported to have anxiolytic actions in man, attenuated only selective aspects of the response to beta-CCE. The behavioral, endocrine, and physiologic effects of low doses of beta-CCE in monkeys are similar to those observed in anxious patients or normal subjects under anxiety-provoking or stressful situations. Administration of benzodiazepine receptor active antagonists such as beta-CCE to primates may, therefore, provide a valid and reproducible model of human anxiety that could be used to investigate specific biologic aspects of anxiety disorders.

Animals↗
PubMed1984

Neuroendocrine responses to apomorphine in depressed patients and healthy control subjects.

Increasing evidence implicates altered dopamine function in major affective illness. In the present study, growth hormone responses to the dopamine agonist apomorphine were not different for 14 male depressed patients and 16 healthy male volunteers. Baseline and post-apomorphine prolactin levels were lower for the depressed patients than the control subjects, but the percent decrease following apomorphine was not different for the two groups. Neuroendocrine responses were not significantly altered during chronic treatment with the dopamine agonist piribedil. These neuroendocrine results suggest that decreased baseline prolactin levels in depressed patients do not reflect altered postsynaptic receptor sensitivity in the tuberoinfundibular dopamine system.

Adult↗
PubMed1984

Disposition and metabolism of MHPG in humans: application to studies in depression.

MHPG is formed from norepinephrine metabolized throughout the body; its levels in plasma reflect total norepinephrine metabolism. Over half of the MHPG, is converted to VMA. Less than 20% of MHPG is derived from brain norepinephrine and urinary excretion of this metabolite cannot be used as a measure of brain norepinephrine metabolism. Because unconjugated MHPG is readily diffusable, there is a free exchange of this metabolite among plasma, cerebrospinal fluid, and nerve tissues (including brain and spinal cord). The CSF MHPG levels, after appropriately correction for the plasma contribution of the metabolite, reflect its rate of formation in the central nervous system.

Adrenal Gland Diseases↗
PubMed1984

Fear and anxiety: relationship to noradrenergic function.

The experiences of human fear and anxiety are discussed within the context of locus ceruleus function in animals. The rationale for studying correlates of noradrenergic function, such as 3-methoxy-4-hydroxyphenethylene glycol (MHPG), is reviewed, and data demonstrating a positive correlation between plasma free MHPG and state anxiety in normal volunteers is presented. The behavioral effects of oral caffeine (240-720 mg), intravenous clonidine (2 micrograms/kg), and oral yohimbine (20 mg) were studied in various psychiatric patients and normal volunteers. Caffeine and yohimbine had anxiogenic properties; conversely, clonidine reduced self-rated measures of anxiety across a wide spectrum of psychiatric conditions. These findings expand previous research indicating that noradrenergic hyperactivity may be associated with many types of human fear and anxiety.

Animals↗
PubMed1984

Differential inhibitory noradrenergic responses to clonidine in 25 depressed patients and 25 normal control subjects.

The authors measured plasma 3-methoxy-4-hydroxyphenylglycol (MHPG), plasma norepinephrine, blood pressure, and heart rate responses to the alpha 2-adrenergic agonist clonidine in 25 depressed patients and 25 normal control subjects. In the control subjects clonidine reduced plasma norepinephrine, blood pressure, and heart rate significantly more than placebo. In the depressed patients clonidine reduced blood pressure and the percent fall in plasma norepinephrine but not plasma MHPG or heart rate significantly more than placebo. The absolute and percent reductions in plasma MHPG and heart rate following clonidine were significantly less than in control subjects. These results raise the possibility that the sensitivity of the alpha 2-adrenergic receptors inhibitory to noradrenergic output may be reduced in depression.

Adult↗
PubMed1984

Chronic autonomic failure: CSF and plasma 3-methoxy-4-hydroxyphenylglycol.

We measured CSF and plasma levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) in patients with orthostatic hypotension. Total CSF MHPG levels were significantly lower than normal in patients with either multiple system atrophy (MSA) or idiopathic orthostatic hypotension (IOH). Only IOH patients had low plasma levels of MHPG. Correction of CSF MHPG levels for the contribution from plasma free MHPG provides an index of central norepinephrine metabolism. In MSA, abnormal function of central noradrenergic pathways seems to cause the low CSF MHPG levels. In IOH, the decreased CSF MHPG results from the diminished plasma MHPG levels.

Adult↗
PubMed1984

Pharmacologic treatment of eating disorders.

Increased research focusing on the eating disorders has put the clinician on firmer ground when choosing appropriate psychopharmacologic treatments. Recent studies of patients with bulimia demonstrate that treatment with antidepressant medications may substantially reduce symptoms of bingeing and vomiting. The efficacy of pharmacologic approaches to anorexia nervosa is more uncertain, in part because of the limited availability of long-term follow-up studies. The judicious use of appetite suppressant medications, as reviewed in the text, is helpful for mild to moderate obesity. In treating these disorders, the clinician needs to integrate medication treatment with psychotherapeutic and behavioral treatment approaches.

Anorexia Nervosa↗