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.
Original language | English (US) |
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Pages (from-to) | 1926-1935 |
Number of pages | 10 |
Journal | Neuropsychopharmacology |
Volume | 34 |
Issue number | 8 |
DOIs | |
State | Published - Jul 2009 |
Keywords
- D2
- GABAB
- IPSC
- Methamphetamine
- Mouse
- Stress
ASJC Scopus subject areas
- Pharmacology
- Psychiatry and Mental health