The (-)-deprenyl actions on beta-adrenergic receptors require the integrity of brain serotonergic axon terminals.

In rats receiving (-)-deprenyl (1 mumol/kg, s.c.) twice daily for 3 weeks, the Bmax of imipramine binding sites located in crude synaptic membranes prepared from frontal cortex increases while the NE stimulation of cAMP accumulation in minces prepared from frontal cortex is attenuated. The presence of intact 5HT axon terminals is an absolute requirement for the down-regulation of the beta-adrenergic receptor function by repeated injections of (-)-deprenyl. These and other lines of evidence suggest that the increase in the Bmax of [3H]imipramine binding sites and the attenuation of beta-adrenergic receptor function elicited by (-)-deprenyl might be causally related.