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Biomedical subjects

G N Pandey

Publications and source records attributed to G N Pandey.

106 records · Page 6Linked to original sources
PubMed1977

Postsynaptic supersensitivity in schizophrenia.

In the context of the dopamine hypothesis of schizophrenia, the authors examined postsynaptic dopamine (DA) receptor sensitivity in schizophrenic patients by means of a neuroendocrine strategy using the DA receptor agonist apomorphine and growth hormone (GH) release as the measurable postsynaptic event. The activity of platelet adenylate cyclase, an enzyme intimately associated with catecholamine receptor activity, was also studied following stimulation by prostaglandin E1 (PGE1). Patients diagnosed as having acute schizophrenia had significantly higher GH responses and adenylate cyclase activity than normal control subjects and patients diagnosed as having chronic schizophrenia. Chronic schizophrenic patients with and without tardive dyskinesia showed GH responses slightly lower than but not significantly different from those of control groups.

Acute Disease↗
PubMed1977

Effects of dopamine agonists in tardive dyskinesia.

The authors used a combined behavioral and neuroendocrinological strategy to investigate the relevance of abnormalities in the brain dopaminergic systems to the pathophysiology of tardive dyskinesia by assessing the effects of apomorphine, a directly acting dopamine agonist, and d-amphetamine, an indirectly acting dopamine agonist, in patients with tardive dyskinesia. Administration of I.V. d-amphetamine increased dyskinetic movements in most patients with tardive dyskinesia, a finding consistent with the dopaminergic hypothesis. Contrary to predictions based on animal models, apomorphine did not increase dyskinetic movements in these patients but instead substantially reduced dyskinesia in some patients. Patients with tardive dyskinesia did not have a greater drop in serum prolactin or a greater rise in serum growth hormone after apomorphine than normal or chronic schizophrenic subjects without tardive dyskinesia.

Administration, Oral↗
PubMed1975

Genetic determinant of lithium ion metabolism. II. An in vivo study of lithium ion distribution across erythrocyte membranes.

A study was conducted to determine if membrane factors, known to influence the distribution of sodium ion (Na) and potassium ion (K), also influence lithium ion distribution. Two groups of sheep with genetically determined differences in their cation concentrations were administered lithium chloride for ten days. The low red blood cell (RBC) potassium ion sheep (LK) had a greater RBC lithium ion concentration than the high RBC potassium ion sheep (HK). In vitro incubation of erythrocytes with lithium chloride also produced substantially different RBC lithium ion: plasma lithium ion ratios similar to those seen in the vivo study. Distribution of lithium ion was generally similar to that of Na ion. It seems that lithium ion distribution may be controlled by the same genetic factors that regulate Na ion distribution.

Animals↗
PubMed1975

Genetic determinant of lithium ion distribution. An in vitro and in vivo monozygotic-dizygotic twin study.

In previous research, evidence was provided of genetic control of in vitro red blood cell (RBC) uptake of lithium ion following a 24-hour incubation using a monozygotic (MZ)-dizygotic (DZ) twin study method. To extend these data, in vitro RBC lithium ion concentrations were assessed for five MZ and five DZ twin pairs. To extend this line of research on genetic control of lithium ion distribution to in vivo conditions, these twin pairs were administered lithium carbonate for seven days during which time RBC and plasma lithium ion concentrations were assessed. In this limited sample, the data provide evidence of genetic control of distribution of lithium ion across the RBC membrane in vivo as well as of in vitro RBC uptake of lithium ion.

Erythrocytes↗
PubMed1975

Growth hormone catecholamines in affective disease.

The authors studied growth hormone (GH) release after insulin-induced hypoglycemia (HI) in relation to urinary MHPG, the major metabolite of central norepinephrine. There was a significant linear correlation of urinary MHPG levels and GH peaks after HI in unipolar depressed patients and in manic patients; however, GH peaks in manic patients shifted downward on the GH axis in comparison to the unipolar depressive patients. The authors suggest that such shifts in the GH response may occur as a result of abnormalities of other neurotransmitter systems also known to facilitate GH release.

Adult↗
PubMedDate not supplied

Beta-adrenergic receptor subtypes in stress-induced behavioral depression.

The purpose of this study was to examine the role of beta-adrenergic receptors in an animal model of stress-induced behavioral depression. beta-Adrenergic receptors in several brain regions and leukocytes of rats were determined by receptor binding techniques using 125I-cyanopindolol (cyp) as ligand and propranolol as displacer for total beta-adrenergic receptors, and ICI 86,406 for beta 1- and ICI 118,551 for beta 2-adrenergic receptors. We observed that the maximum number of binding sites (Bmax) and the apparent dissociation constant (Kd) of 125I-cyp binding to total beta-adrenergic receptors were increased in hippocampus of stressed rats with escape deficits (48 h after training) as compared to control rats. This increase was due to an increase in Bmax and Kd of 125I-cyp binding to beta 1-adrenergic receptors but not to beta 2-adrenergic receptors. There was no significant difference in beta 1-adrenergic receptors in cortex and cerebellum or beta 2-adrenergic receptors in hippocampus, cortex, cerebellum, or leukocytes of stressed (48 h after training) rats with escape deficits as compared to control rats. Interestingly, it was observed that beta 1- and beta 2-adrenergic receptors in various brain regions (cortex, cerebellum, and hippocampus) and beta 2-adrenergic receptors in leukocytes of stressed rats (10 days after training) were not significantly different from control rats, although escape deficits were still present. These results suggest that abnormalities in adrenergic neurotransmission are associated with an upregulation of beta 1-adrenergic receptors, which in turn may be involved in the early stages of behavioral deficits caused by uncontrollable shock.

Animals↗
PubMedDate not supplied

Chronic ethanol consumption decreases the phorbol ester binding to membranal but not cytosolic protein kinase C in rat brain.

We examined the effect of 60 days of ethanol treatment on protein kinase C (PKC) in membrane and cytosolic fractions of the rat cerebral cortex. Membranal and cytosolic PKC were determined by binding technique using [3H]-phorbol 12,13 dibutyrate (PDBU) as radioligand and phorbol 12-myristate 13-acetate (PMA) as displacer. Chronic ethanol consumption resulted in a decrease in the maximum number of binding sites (Bmax) of [3H]-PDBU binding to membranal PKC without significant change in the apparent dissociation constant (KD) in the rat cortex. We also observed that chronic ethanol consumption had no significant effect on Bmax or KD of [3H]-PDBU binding to cytosolic PKC in the rat cerebral cortex. These results suggest that chronic ethanol consumption leads to the down-regulation of brain PKC associated with membrane but not with cytosol.

Alcoholism↗
PubMedDate not supplied

Chronic ethanol effects on the expression of phospholipase C isozymes and Gq/11-protein in primary cultures of astrocytes.

The goal of this investigation was to determine whether chronic ethanol exposure alters the expression of specific protein sites distal to receptors [Gq/11-protein, phospholipase C (PLC) isozymes] in primary cultures of astrocytes obtained from neonatal rat cortex. The protein expression (immunolabeling) of the PLC-beta 1, -gamma 1, -delta 1 isozymes and of the Gq/11 alpha subunit was determined by Western blot analysis using specific monoclonal antibodies. The PLC-beta 1, -gamma 1, -delta 1 isozymes and the Gq/11 alpha subunit migrated at apparent molecular masses (PLC-beta 1, 41 kDa; PLC-gamma 1, 145 kDa. PLC-delta 1, 85 kDa: Gq/11 alpha protein, 42 kDa). Thus, a PLC-beta 1 fragment of 41 kDa, but not the biologically active 150 kDa PLC-beta 1, was detected in primary cultures of astrocytes. Chronic ethanol exposure (4 days) resulted in a significant increase in the expression of PLC-delta 1, whereas under identical conditions, the expression of PLC-beta 1, -gamma 1, and of the alpha subunit of Gq/11 protein was not significantly altered in astrocytes. These results suggest that chronic ethanol exposure results in an increased expression of the PLC-delta 1, isozyme in primary cultures of astrocytes.

Animals↗
PubMedDate not supplied

Stress-induced desensitization of alpha 2-adrenergic receptors in human platelets.

Although agonist-induced desensitization of adrenergic receptors has been previously demonstrated, the regulation of adrenergic receptors during acute psychological stress has not been investigated in humans. We studied 30 first year medical students during final examination week and one month earlier. Platelet alpha 2 receptor binding was measured using 3H-yohimbine and leukocyte beta 2 receptor binding was measured with 125I-CYP (Iodocyanopindolol). During final examination week, platelet alpha 2-receptor binding affinity was significantly reduced, while levels of plasma catecholamines and reported anxiety were significantly increased, compared with the earlier period. Students showing the greatest increases in plasma norepinephrine and in reported anxiety also demonstrated the greatest reductions in alpha 2 receptor binding affinity. These data show that acute psychological stress can produce adrenergic receptor desensitization, possibly through increased levels of circulating norepinephrine.

Adult↗