Competitive regulation of synaptic Ca2+ influx by D2 dopamine and A2A adenosine receptors.

ABSTRACT: Striatal D2-type dopamine receptors (D2Rs) have been implicated in the pathophysiology of neuropsychiatric disorders, including Parkinson's disease and schizophrenia. Although these receptors regulate striatal synaptic plasticity, the mechanisms underlying dopaminergic modulation of glutamatergic synapses are unclear. We combined optogenetics, two-photon microscopy and glutamate uncaging to examine D2R-dependent modulation of glutamatergic synaptic transmission in mouse striatopallidal neurons. We found that D2R activation reduces corticostriatal glutamate release and attenuates both synaptic- and action potential-evoked Ca2+ influx into dendritic spines by approximately 50%. Modulation of Ca2+ signaling was mediated by a protein kinase A (PKA)-dependent regulation of Ca2+ entry through NM

SUBMITTER: Higley MJ 

PROVIDER: S-EPMC2910780 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature