Journal
BEHAVIOR GENETICS
Volume 39, Issue 1, Pages 62-72Publisher
SPRINGER
DOI: 10.1007/s10519-008-9232-1
Keywords
TRPV1 receptor; Knockout mice; Ethanol; Trigeminal; Sensory behavior
Funding
- NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [R01AA015741] Funding Source: NIH RePORTER
- NIAAA NIH HHS [R01 AA015741, R01 AA015741-02, AA015741] Funding Source: Medline
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Ethanol is a known oral trigeminal stimulant and recent data indicate that these effects are mediated in part by transient receptor potential channel vanilloid receptor 1 (TRPV1). The importance of this receptor in orally mediated ethanol avoidance is presently unknown. Here, we compared orosensory responding to ethanol in TRPV1-deficient and wild type mice in a brief-access paradigm that assesses orosensory influences by measuring immediate licking responses to small stimulus volumes. TRPV1(-/-) and control mice were tested with six concentrations of ethanol (3, 5, 10, 15, 25, 40%), capsaicin (0.003, 0.01, 0.03, 0.1, 0.3, 1 mM), sucrose (0.003, 0.01, 0.03, 0.1, 0.3, 1 M), and quinine (0.01, 0.03, 0.1, 0.3, 1, 3 mM) and psychophysical concentration-response functions were generated for each genotype and stimulus. TRPV1 knockouts displayed reduced oral avoidance responses to ethanol regardless of concentration, insensitivity to capsaicin, and little to no difference in sweet or bitter taste responding relative to wild type mice. These data indicate that the TRPV1 channel plays a role in orosensory-mediated ethanol avoidance, but that other receptor mechanisms likely also contribute to aversive oral responses to alcohol.
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