{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,6,25]],"date-time":"2025-06-25T05:25:02Z","timestamp":1750829102973},"reference-count":70,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,10,12]],"date-time":"2004-10-12T00:00:00Z","timestamp":1097539200000},"content-version":"vor","delay-in-days":3694,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Synapse"],"published-print":{"date-parts":[[1994,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The effect of long\u2010term (6\u201319 weeks) 6\u2010hydroxydopamine\u2010induced (6\u2010OHDA) lesions of midbrain dopamine cells on dopamine D<jats:sub>1<\/jats:sub>\u2010like agonist\u2010induced changes in the excitability of rat striatal neurons was investigated in vitro using tissue slices and intracellular recording techniques. Fenoldopam and (\u00b1)\u2010SKF 38393 predominantly decreased excitability in control preparations including striatal neurons located contralateral to 6\u2010OHDA injection sites and neurons obtained from rats receiving sham injections or no treatment. Fenoldopam also inhibited neurons ipsilateral to lesions of midbrain dopamine cells. (\u00b1)\u2010SKF 33393, unlike fenoldopam, produced predominantly increases in the excitability of ipsilateral striatal neurons. Superfusion of the D<jats:sub>1<\/jats:sub> receptor antagonist, SCH 23390, blocked fenoldopam\u2010induced decreases in excitability but not the (\u00b1)\u2010SKF 38393\u2010induced excitation of neurons ipsilateral to the lesion. Sequential application of fenoldopam and quinpirole, a D<jats:sub>2<\/jats:sub>\/D<jats:sub>3<\/jats:sub> receptor agonist, produced responses to both drugs in a majority of neurons. The results demonstrate that inhibitory responses to fenoldopam are mediated by D<jats:sub>1<\/jats:sub> receptors, while excitatory effects of (\u00b1)\u2010SKF 38393 in the striatum ipsilateral to the lesion are apparently not dependent on D<jats:sub>1<\/jats:sub> receptor activation. These findings also suggest that dopamine D<jats:sub>1<\/jats:sub> and D2\/D3 receptors are able to concurrently influence the excitability of striatal neurons in the dopamine deafferentated striatum. Similar regulation of striatal neurons in vivo may contribute to dopaminergic regulation of basal ganglia output and the ability of dopaminomimetic agents to ameliorate symptoms of dopaminergic deficiency in Parkinson's disease. \u00a9 1994 Wiley\u2010Liss, Inc.<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"#fn1\" \/><jats:fn><jats:p>This article is a US Government work and, as such, is in the public domain in the United States of America.<\/jats:p><\/jats:fn>\n<\/jats:p>","DOI":"10.1002\/syn.890180109","type":"journal-article","created":{"date-parts":[[2004,12,31]],"date-time":"2004-12-31T22:21:54Z","timestamp":1104531714000},"page":"67-78","source":"Crossref","is-referenced-by-count":6,"title":["Intracellularly recorded response of rat striatal neurons in vitro to fenoldopam and SKF 38393 following lesions of midbrain dopamine cells"],"prefix":"10.1002","volume":"18","author":[{"given":"M. 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