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Serotonin-2C receptor agonists decrease potassium-stimulated GABA release in the nucleus accumbens.

James M Kasper1, Raymond G Booth, Joanna Peris

  • 1Department of Pharmacology and Toxicology, University of Texas-Medical Branch, Galveston, Texas, 77555.

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|November 11, 2014
PubMed
Summary
This summary is machine-generated.

Serotonin 5-HT2C receptor agonists reduce alcohol seeking by decreasing GABA release in the nucleus accumbens. This finding offers a potential mechanism for treating alcoholism.

Keywords:
5-HT2C receptorGABAcapillary electrophoresismicrodialysisnucleus accumbens

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Addiction Research

Background:

  • The serotonin 5-HT2C receptor is a potential therapeutic target for alcoholism.
  • Previous research indicates 5-HT2C receptor agonism activates GABA neurons in the ventral tegmental area (VTA).
  • The effect of 5-HT2C receptor modulation on GABA release in the nucleus accumbens core (NAcc) remains unclear.

Purpose of the Study:

  • To investigate the impact of 5-HT2C receptor modulation on GABA release in the NAcc.
  • To explore the mechanism underlying the anti-alcoholism effects of 5-HT2C receptor agonists.

Main Methods:

  • Microdialysis coupled with capillary electrophoresis and laser-induced fluorescence was employed.
  • Extracellular neurotransmitter concentrations in the NAcc were quantified in rats.
  • Effects of 4-phenyl-2-N,N-dimethylaminotetralin (PAT) analogs and other 5-HT2C modulators were assessed via reverse dialysis.

Main Results:

  • 5-HT2C receptor agonists specifically attenuated stimulated GABA release in the NAcc.
  • 5-HT2C antagonists or inverse agonists did not affect GABA release.
  • Agents acting on 5-HT2A receptors showed no impact on GABA release.

Conclusions:

  • 5-HT2C receptor agonists decrease stimulated GABA release in the NAcc.
  • This finding contrasts with previous VTA studies and suggests a novel mechanism for modulating alcohol self-administration.
  • The results provide a potential neurobiological basis for 5-HT2C-mediated reduction in ethanol intake.