Opposing actions of CRF-R1 and CB1 receptors on VTA-GABAergic plasticity following chronic exposure to ethanol.

ABSTRACT: Dopamine neurons in the ventral tegmental area (VTA) influence learned behaviors and neuropsychiatric diseases including addiction. The stress peptide corticotrophin-releasing factor (CRF) contributes to relapse to drug and alcohol seeking following withdrawal, although the cellular actions are poorly understood. In this study, we show that presynaptic CRF type 1 receptors (CRF-R1) potentiate GABA release onto mouse VTA dopamine neurons via a PKC-Ca²⁺ signaling mechanism. In naive animals, activation of CRF-R1 by bath application of CRF or ethanol enhanced GABA_A inhibitory postsynaptic currents (IPSCs). Following 3 days of withdrawal from four weekly cycles of chronic intermittent ethanol (CIE) vapor exposure, spontaneous IPSC frequency was enhanced while CRF and etha

SUBMITTER: Harlan BA 

PROVIDER: S-EPMC6098046 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature