BETA-ADRENERGIC-RECEPTOR SUBTYPES IN STRESS-INDUCED BEHAVIORAL DEPRESSION

Citation
Sc. Pandey et al., BETA-ADRENERGIC-RECEPTOR SUBTYPES IN STRESS-INDUCED BEHAVIORAL DEPRESSION, Pharmacology, biochemistry and behavior, 51(2-3), 1995, pp. 339-344
Citations number
38
Categorie Soggetti
Pharmacology & Pharmacy","Pharmacology & Pharmacy
ISSN journal
00913057
Volume
51
Issue
2-3
Year of publication
1995
Pages
339 - 344
Database
ISI
SICI code
0091-3057(1995)51:2-3<339:BSISBD>2.0.ZU;2-H
Abstract
The purpose of this study was to examine the role of beta-adrenergic r eceptors in an animal model of stress-induced behavioral depression. b eta-Adrenergic receptors in several brain regions and leukocytes of ra ts were determined by receptor binding techniques using I-125-cyanopin dolol (cyp) as ligand and propranolol as displacer for total beta-adre nergic receptors, and ICI 86,406 for beta(1)- and ICI 118,551 for beta (2)-adrenergic receptors. We observed that the maximum number of bindi ng sites (B-max) and the apparent dissociation constant (K-d) of I-125 -cyp binding to total beta-adrenergic receptors were increased in hipp ocampus of stressed rats with escape deficits (48 h after training) as compared to control rats. This increase was due to an increase in B-m ax and K-d of I-125-cyp binding to beta(1)-adrenergic receptors but no t to beta(2)-adrenergic receptors. There was no significant difference in beta(1)-adrenergic receptors in cortex and cerebellum or beta(2)-a drenergic receptors in hippocampus, cortex, cerebellum, or leukocytes of stressed (48 h after training) rats with escape deficits as compare d to control rats. Interestingly, it was observed that beta(1)- and be ta(2)-adrenergic receptors in various brain regions (cortex, cerebellu m, and hippocampus) and beta(2)-adrenergic receptors in leukocytes of stressed rats (10 days after training) were not significantly differen t from control rats, although escape deficits were still present. Thes e results suggest that abnormalities in adrenergic neurotransmission a re associated with an upregulation of beta(1)-adrenergic receptors, wh ich in turn may be involved in the early stages of behavioral deficits caused by uncontrollable shock.