Loss of β-arrestin2 in D2 cells alters neuronal excitability in the nucleus accumbens and behavioral responses to psychostimulants and opioids.

ABSTRACT: Psychostimulants and opioids increase dopamine (DA) neurotransmission, activating D1 and D2 G protein-coupled receptors. β-arrestin2 (βarr2) desensitizes and internalizes these receptors and initiates G protein-independent signaling. Previous work revealed that mice with a global or cell-specific knockout of βarr2 have altered responses to certain drugs; however, the effects of βarr2 on the excitability of medium spiny neurons (MSNs), and its role in mediating the rewarding effects of drugs of abuse are unknown. D1-Cre and D2-Cre transgenic mice were crossed with floxed βarr2 mice to eliminate βarr2 specifically in cells containing either D1 (D1^βarr2-KO ) or D2 (D2^βarr2-KO ) receptors. We used slice electrophysiology to characterize the role of βarr2 in modulating D1

SUBMITTER: Porter-Stransky KA 

PROVIDER: S-EPMC7035979 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature