ALPHA-2-ADRENOCEPTORS ARE NOT INVOLVED IN THE REGULATION OF STRIATAL GLUTAMATE RELEASE - COMPARISON TO DOPAMINERGIC INHIBITION

Striatal slices from the rat were loaded with [H-3]glutamate ([H-3]Glu) and superfused in order to measure release of radioactivity at rest and during potassium-evoked depolarization. Addition of KCl (22-40 mmol/liter) to the perfusion fluid enhanced the release of tritium in a concentration-dependent manner, and this release was abolished by omission of CaCl2. High-performance liquid chromatography (HPLC) separation coupled with radiochemical detection revealed that 23% and 41% of the tritium efflux detected in the perfusion fluid under resting conditions and during potassium stimulation, respectively, was due to [H-3]Glu. At the end of the superfusion about 63% of residual tritium content in the tissue was [H-3]Glu. Tritium efflux in response to KCl excess was significantly higher from striatum dissected from 6-hydroxydopamine-pretreated rats. Apomorphine decreased the KCl-evoked release of [H-3]Glu, and haloperidol exerted the opposite effect. Yohimbine, which antagonized the decrease of dopa accumulation elicited by apomorphine in NSD-1015 and gamma-butyrolactone-pretreated rat caudate nucleus, also reversed the apomorphine inhibition of the release of [H-3]Glu evoked by depolarization. The selective alpha-2-adrenoceptor antagonist CH-38083, however, did not modify the apomorphine inhibition of [H-3]Glu release or dopa accumulation, and the alpha-2-adrenoceptor agonist xylazine did not alter tritium efflux from striatum preloaded with [H-3]Glu. These findings suggest that release of glutamate (Glu) from the corticostriatal pathway is under tonic control of dopamine released from nigrostriatal neurons, and alpha-2-adrenoceptors are not involved in the regulation of glutamatergic transmission in the rat striatum. The effect of yohimbine on Glu release is attributed to its antidopaminergic rather than alpha-2-adrenoceptor blocking effect.