Referenced in: none

Automatically associated channels: Slo1

Title: CRF enhancement of GIRK channel-mediated transmission in dopamine neurons.

Authors: Michael J Beckstead, Stephanie C Gantz, Christopher P Ford, Mary P Stenzel-Poore, Paul Em Phillips, Gregory P Mark, John T Williams

Journal, date & volume: Neuropsychopharmacology, 2009 Jul , 34, 1926-35

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/19279570

Abstract
Dopamine neurons in the ventral midbrain contribute to learning and memory of natural and drug-related rewards. Corticotropin-releasing factor (CRF), a stress-related peptide, is thought to be involved in aspects of relapse following drug withdrawal, but the cellular actions are poorly understood. This study investigates the action of CRF on G-protein-linked inhibitory postsynaptic currents (IPSCs) mediated by GIRK (Kir3) channels in dopamine neurons. CRF enhanced the amplitude and slowed the kinetics of IPSCs following activation of D2-dopamine and GABA(B) receptors. This action was postsynaptic and dependent on the CRF(1) receptor. The enhancement induced by CRF was attenuated by repeated in vivo exposures to psychostimulants or restraint stress. The results indicate that CRF influences dopamine- and GABA-mediated inhibition in the midbrain, suggesting implications for the chronic actions of psychostimulants and stress on dopamine-mediated behaviors.