Striatal slices from the rat were loaded with [3H]glutamate ([3H]Glu) superfused measure release of radioactivity at rest and during potassium‐evoked depolarization. Addition of KC1 (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 delection revealed that 23% and 41% of the tritium efflux detected in the perfusion fluid under resting conditions and during potassium stimulation, respec‐lively, was due to [3H]Glu. At the end of the super‐fusion about 63% of residual tritium content in the tissue was [3H]Glu. Tritium efflux in response to KCI excess was significantly higher from striatum dissected from 6‐hydroxydopamine‐pretreated rats. Apomorphine decreased, the KCl‐evoked release of [3H]Glu haloperidol exerted the opposite effect, Yohimbine, which antagonized the decrease of dopa accumulation elicited by apomorphine in NSD‐1015 and γ‐butyrolactone‐pretreated rat caudate nucleus, also reversed the appmprphine inhibition of the, re‐lease of [3H]Glu evoked by depolarization. The selective α2‐adrenoceptor antagonist CH‐38083, however, did not modify the apomorphine inhibition of [3H]GIu release or dopa accumulation, andthe α2‐adrenoceptor agonist xylazine did not alter tritium efflux from striatum preloaded with [3H]Glu. These findings suggest that release of glutamate (Glu) from the corticostriatal pathway is under tonic control of dopamine released from nigrostriatal neurons, and α2‐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 α2 adrenoceptor blocking effect.
- high‐performance liquid chromatography
- rat striatum
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience