CRF enhancement of GIRK channel-mediated transmission in dopamine neurons

Michael J. Beckstead, Stephanie C. Gantz, Christopher P. Ford, Mary P. Stenzel-Poore, Paul E.M. Phillips, Gregory P. Mark, John T. Williams

Research output: Contribution to journalArticlepeer-review

48 Scopus citations


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 languageEnglish (US)
Pages (from-to)1926-1935
Number of pages10
Issue number8
StatePublished - Jul 2009


  • D2
  • IPSC
  • Methamphetamine
  • Mouse
  • Stress

ASJC Scopus subject areas

  • Pharmacology
  • Psychiatry and Mental health


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