Selective Ablation of GIRK Channels in Dopamine Neurons Alters Behavioral Effects of Cocaine in Mice.

ABSTRACT: The increase in dopamine (DA) neurotransmission stimulated by in vivo cocaine exposure is tempered by G protein-dependent inhibitory feedback mechanisms in DA neurons of the ventral tegmental area (VTA). G protein-gated inwardly rectifying K⁺ (GIRK/Kir3) channels mediate the direct inhibitory effect of GABA_B receptor (GABA_BR) and D₂ DA receptor (D₂R) activation in VTA DA neurons. Here we examined the effect of the DA neuron-specific loss of GIRK channels on D₂R-dependent regulation of VTA DA neuron excitability and on cocaine-induced, reward-related behaviors. Selective ablation of Girk2 in DA neurons did not alter the baseline excitability of VTA DA neurons but significantly reduced the magnitude of D₂R-dependent

SUBMITTER: McCall NM 

PROVIDER: S-EPMC5240170 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature