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Marked decrease of LSD-induced stimulus control in serotonin transporter knockout mice.

C M Krall1, J B Richards, R A Rabin

  • 1Department of Pharmacology and Toxicology, School of Medicine and Biomedical Sciences, University at Buffalo, 102 Farber Hall, SUNY-Buffalo, NY 14214-3000, USA.

Pharmacology, Biochemistry, and Behavior
|October 16, 2007
PubMed
Summary
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Mice lacking the serotonin transporter (SERT) show reduced stimulus control by LSD, indicating that SERT is crucial for LSD

Area of Science:

  • Neuroscience
  • Pharmacology
  • Genetics

Background:

  • LSD stimulus control is primarily mediated by 5-HT2A receptors, with 5-HT1A and 5-HT2C subtypes playing modulatory roles.
  • Mice lacking the serotonin transporter (SERT) exhibit decreased 5-HT2A receptor density and reduced 5-HT2A receptor function.
  • This suggests that LSD's efficacy in establishing stimulus control may be impaired in SERT knockout mice.

Purpose of the Study:

  • To investigate the efficacy of LSD in establishing stimulus control in SERT knockout (KO) mice.
  • To compare LSD's effects with a non-serotonergic drug, pentobarbital, in SERT KO and wildtype (WT) mice.

Main Methods:

  • SERT KO and WT mice were trained on a visual discrimination task.
  • Subsequent training involved administering LSD (0.17 or 0.30 mg/kg) or vehicle.

Related Experiment Videos

  • Pentobarbital (15 or 30 mg/kg) or vehicle was used to control for general drug discrimination deficits.

    • Main Results:

    • The visual stimulus controlled behavior in both WT and SERT KO mice.
    • LSD established stimulus control in 90% of WT mice but only 31% of SERT KO mice.
    • Pentobarbital established stimulus control in 80% of WT mice and 54% of SERT KO mice.

    Conclusions:

    • SERT KO mice show significantly reduced stimulus control by LSD compared to WT mice.
    • These findings suggest that reduced 5-HT1A and/or 5-HT2A receptor density in SERT KO mice underlies the diminished efficacy of LSD.
    • SERT plays a critical role in mediating LSD's stimulus control effects.