{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,10]],"date-time":"2025-09-10T22:46:20Z","timestamp":1757544380719},"reference-count":25,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2004,10,11]],"date-time":"2004-10-11T00:00:00Z","timestamp":1097452800000},"content-version":"vor","delay-in-days":4973,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[1991,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Striatal slices from the rat were loaded with [<jats:sup>3<\/jats:sup>H]glutamate ([<jats:sup>3<\/jats:sup>H]Glu) superfused measure release of radioactivity at rest and during potassium\u2010evoked depolarization. Addition of KC1 (22\u201040 mmol\/liter) to the perfusion fluid enhanced the release of tritium in a concentration\u2010dependent manner, and this release was abolished by omission of CaCl<jats:sub>2<\/jats:sub>. High\u2010performance 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\u2010lively, was due to [<jats:sup>3<\/jats:sup>H]Glu. At the end of the super\u2010fusion about 63% of residual tritium content in the tissue was [<jats:sup>3<\/jats:sup>H]Glu. Tritium efflux in response to KCI excess was significantly higher from striatum dissected from 6\u2010hydroxydopamine\u2010pretreated rats. Apomorphine decreased, the KCl\u2010evoked release of [<jats:sup>3<\/jats:sup>H]Glu haloperidol exerted the opposite effect, Yohimbine, which antagonized the decrease of dopa accumulation elicited by apomorphine in NSD\u20101015 and \u03b3\u2010butyrolactone\u2010pretreated rat caudate nucleus, also reversed the appmprphine inhibition of the, re\u2010lease of [<jats:sup>3<\/jats:sup>H]Glu evoked by depolarization. The selective \u03b1<jats:sub>2<\/jats:sub>\u2010adrenoceptor antagonist CH\u201038083, however, did not modify the apomorphine inhibition of [<jats:sup>3<\/jats:sup>H]GIu release or dopa accumulation, andthe \u03b1<jats:sub>2<\/jats:sub>\u2010adrenoceptor agonist xylazine did not alter tritium efflux from striatum preloaded with [<jats:sup>3<\/jats:sup>H]Glu. These findings suggest that release of glutamate (Glu) from the corticostriatal pathway is under tonic control of dopamine released from nigrostriatal neurons, and \u03b1<jats:sub>2<\/jats:sub>\u2010adrenoceptors 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 \u03b1<jats:sub>2<\/jats:sub> adrenoceptor blocking effect.<\/jats:p>","DOI":"10.1002\/jnr.490280309","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T05:43:57Z","timestamp":1104558237000},"page":"376-381","source":"Crossref","is-referenced-by-count":15,"title":["\u03b1<sub>2<\/sub>\u2010Adrenoceptors are not involved in the regulation of striatal glutamate release: Comparison to dopaminergic inhibition"],"prefix":"10.1002","volume":"28","author":[{"suffix":"Jr","given":"L. G.","family":"Harsing","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E. 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