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J Neurophysiol 87: 2167-2175, 2002;
0022-3077/02 $5.00
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The Journal of Neurophysiology Vol. 87 No. 4 April 2002, pp. 2167-2175
Copyright ©2002 by the American Physiological Society

D1/D5 Dopamine Receptors Stimulate Intracellular Calcium Release in Primary Cultures of Neocortical and Hippocampal Neurons

Nelson Lezcano and Clare Bergson

Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912-2300

Lezcano, Nelson and Clare Bergson. D1/D5 Dopamine Receptors Stimulate Intracellular Calcium Release in Primary Cultures of Neocortical and Hippocampal Neurons. J. Neurophysiol. 87: 2167-2175, 2002. 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 Gq/11-coupled G-protein-coupled receptor (GPCR) agonists, the typically Gs-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<UP><SUB>i</SUB><SUP>2+</SUP></UP>) levels. The D1/D5 receptor stimulated responses occurred in the absence of extracellular Ca2+ indicating the rises in Ca<UP><SUB>i</SUB><SUP>2+</SUP></UP> 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 Gq/11-coupled glutamate, serotonin, muscarinic, and adrenergic receptors or with high external K+ solution. In contrast, D1/D5 receptor agonist-evoked Ca2+ 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 Ca2+ response in neocortical neurons indicating that increased cAMP levels are not sufficient to stimulate Ca<UP><SUB>i</SUB><SUP>2+</SUP></UP> release. Our data suggest that D1-like dopamine receptors likely modulate neocortical and hippocampal neuronal excitability and synaptic function via Ca2+ as well as cAMP-dependent signaling.




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