Reduced central noradrenergic function has been implicated as a factor
in reduced behavioral activity after stress. The present studies exam
ined the role of reduced beta adrenergic neurotransmission in mediatin
g this effect. This was done by testing the ability of beta receptor a
ntagonists to mimic the behavioral actions of stress. Mice were subjec
ted to stress or given various beta antagonists and tested for swimmin
g behavior, locomotor activity, or grooming behavior. As previously re
ported, stress reduced swimming and locomotor activity and increased g
rooming. Both the nonselective antagonist, l-propranolol, and the beta
-1 selective antagonist, betaxolol, produced the same effects as stres
s on all three measures. A beta-2 selective antagonist, ICI 118,551, w
as effective only on swimming, whereas a membrane stabilizing agent, d
-propranolol, was effective only on grooming behavior. The peripherall
y active beta-1 antagonist, atenolol, was not effective on any measure
. The nonspecific dopaminergic receptor blocker, fluphenazine, reduced
locomotion but tended also to reduce grooming. The results indicate t
hat blockade of beta-1 receptors in the CNS selectively mimics the act
ion of stress on gross motor activity in mice and, along with previous
data, suggest that stress leads to a relative deficiency in central b
eta-1 noradrenergic neurotransmission in these animals.