Pandey S C, Ren X, Sagen J, Pandey G N
Department of Psychiatry, College of Medicine, University of Illinois at Chicago 60612, USA.
Pharmacol Biochem Behav. 1995 Jun-Jul;51(2-3):339-44. doi: 10.1016/0091-3057(94)00392-v.
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.
