IN-VIVO EVIDENCE THAT NONNEURONAL BETA-ADRENOCEPTORS AS WELL AS DOPAMINE-RECEPTORS CONTRIBUTE TO CYCLIC-AMP EFFLUX IN RAT STRIATUM

We applied in vivo microdialysis to assess the effects of dopaminergic and beta-adrenergic receptor stimulation on cyclic AMP efflux in rat striatum under chloral hydrate anesthesia. Dopamine (up to 1 mM) infus ed for 20 min through the probe did not increase cyclic AMP, whereas b oth the selective dopamine D-1 agonist SKF 38393 and D-2 antagonist su lpiride produced modest increases. It is interesting that the beta-adr enoceptor agonist isoproterenol produced a marked increase (204.7% of basal level at 1 mM) which was antagonized by the beta-adrenoceptor an tagonist propranolol. Pretreatment with a glial selective metabolic in hibitor, fluorocitrate (1 mM), by a 5-h infusion through the probe att enuated basal cyclic AMP efflux by 30.3% and significantly blocked the response to isoproterenol. By contrast, striatal injection of a neuro toxin, kainic acid (2.5 mu g), 2 days before the dialysis experiment d id not affect basal cyclic AMP or the response to isoproterenol, but b locked the response to SKF 38393. These data demonstrate that beta-adr enoceptors as well as dopamine receptors contribute to cyclic AMP effl ux in rat striatum in vivo. They also suggest that basal and beta-adre noceptor-stimulated cyclic AMP efflux are substantially dependent on i ntact glial cells.