{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T05:14:38Z","timestamp":1791868478443,"version":"4.3.4"},"reference-count":63,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2002,4,1]]},"abstract":"<jats:p>D1\/D5 dopamine receptors in basal ganglia, hippocampus, and cerebral cortex modulate motor, reward, and cognitive behavior. Previous work with recombinant proteins revealed that in cells primed with heterologous G<jats:sub>q\/11<\/jats:sub>-coupled G-protein-coupled receptor (GPCR) agonists, the typically G<jats:sub>s<\/jats:sub>-linked D1\/D5 receptors can stimulate robust release of calcium from internal stores when coexpressed with calcyon. To learn more about the intracellular signaling mechanisms underlying these D1\/D5 receptor regulated behaviors, we explored the possibility that endogenous receptors stimulate internal release of calcium in neurons. We have identified a population of neurons in primary cultures of hippocampus and neocortex that respond to D1\/D5 dopamine receptor agonists with a marked increase in intracellular calcium (Ca[Formula: see text]) levels. The D1\/D5 receptor stimulated responses occurred in the absence of extracellular Ca<jats:sup>2+<\/jats:sup>indicating the rises in Ca[Formula: see text] involve release from internal stores. In addition, the responses were blocked by D1\/D5 receptor antagonists. Further, the D1\/D5 agonist-evoked responses were state dependent, requiring priming with agonists of G<jats:sub>q\/11<\/jats:sub>-coupled glutamate, serotonin, muscarinic, and adrenergic receptors or with high external K<jats:sup>+<\/jats:sup>solution. In contrast, D1\/D5 receptor agonist-evoked Ca<jats:sup>2+<\/jats:sup>responses were not detected in neurons derived from striatum. However, D1\/D5 agonists elevated cAMP levels in striatal cultures as effectively as in neocortical and hippocampal cultures. Further, neither forskolin nor 8-Br-cAMP stimulation following priming was able to mimic the D1\/D5 agonist-evoked Ca<jats:sup>2+<\/jats:sup>response in neocortical neurons indicating that increased cAMP levels are not sufficient to stimulate Ca[Formula: see text] release. Our data suggest that D1-like dopamine receptors likely modulate neocortical and hippocampal neuronal excitability and synaptic function via Ca<jats:sup>2+<\/jats:sup>as well as cAMP-dependent signaling.<\/jats:p>","DOI":"10.1152\/jn.00541.2001","type":"journal-article","created":{"date-parts":[[2016,7,29]],"date-time":"2016-07-29T00:47:16Z","timestamp":1469753236000},"page":"2167-2175","source":"Crossref","is-referenced-by-count":88,"title":["D1\/D5 Dopamine Receptors Stimulate Intracellular Calcium Release in Primary Cultures of Neocortical and Hippocampal Neurons"],"prefix":"10.1152","volume":"87","author":[{"given":"Nelson","family":"Lezcano","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912-2300"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clare","family":"Bergson","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, Medical College of 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