Journal article
CRF Enhancement of GIRK Channel-Mediated Transmission in Dopamine Neurons
Neuropsychopharmacology (New York, N.Y.), Vol.34(8), pp.1926-1935
07/2009
DOI: 10.1038/npp.2009.25
PMCID: PMC3640552
PMID: 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.
Details
- Title: Subtitle
- CRF Enhancement of GIRK Channel-Mediated Transmission in Dopamine Neurons
- Creators
- Michael J Beckstead - Department of Behavioral Neuroscience, Oregon Health and Science University, Portland, OR, USAStephanie C Gantz - Vollum Institute, Oregon Health and Science University, Portland, OR, USAChristopher P Ford - Vollum Institute, Oregon Health and Science University, Portland, OR, USAMary P Stenzel-Poore - Department of Molecular Microbiology and Immunology, Oregon Health and Science University, Portland, OR, USAPaul EM Phillips - Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA, USAGregory P Mark - Department of Behavioral Neuroscience, Oregon Health and Science University, Portland, OR, USAJohn T Williams - Vollum Institute, Oregon Health and Science University, Portland, OR, USA
- Resource Type
- Journal article
- Publication Details
- Neuropsychopharmacology (New York, N.Y.), Vol.34(8), pp.1926-1935
- DOI
- 10.1038/npp.2009.25
- PMID
- 19279570
- PMCID
- PMC3640552
- ISSN
- 0893-133X
- eISSN
- 1740-634X
- Grant note
- K01 DA021699 || DA / National Institute on Drug Abuse : NIDA R01 DA004523 || DA / National Institute on Drug Abuse : NIDA
- Language
- English
- Date published
- 07/2009
- Academic Unit
- Molecular Physiology and Biophysics; Iowa Neuroscience Institute
- Record Identifier
- 9984065371702771
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