Sc. Pandey et al., BETA-ADRENERGIC-RECEPTOR SUBTYPES IN STRESS-INDUCED BEHAVIORAL DEPRESSION, Pharmacology, biochemistry and behavior, 51(2-3), 1995, pp. 339-344
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.