Simple behavioral methods to assess the effect of drugs or toxins on sensory experience.

When behavioral pharmacologists/toxicologists study conditioned taste aversions (CTAs), or other conditioned responses, as a means to investigate the effects of various drugs or toxins on a learned response, failure to discover a CTA is frequently attributed to the treatment's influence on the associative process. This kind of analysis may fail to identify drug-induced sensory changes that may influence conditioned stimulus (CS) or unconditioned stimulus (US) saliency. The current paper outlines a simple method by which a drug's influence on CS or US sensation may be determined. Further, illustrative data are provided regarding how N-methyl-D-aspartate (NMDA) receptor blockade modulates taste and the sensation of malaise. Ketamine (an NMDA receptor antagonist) has been reported to block CTAs in both neonatal and adult rats. The current experiments evaluated ketamine's ability to modulate the taste of a frequently employed CS (saccharin HCl=SAC) or the aversive aspects of a common US (Lithium Chloride=LiCl). Rats normally exhibit a preference for 0.3% SAC over 0.6% SAC and will suppress consumption of these liquids following an injection of LiCl. We report that ketamine did not markedly antagonize these consummatory patterns nor did it disrupt spontaneous locomotor movements. Taken together, these findings point to ketamine's limited ability to change the sensory capacities required for CTA formation. Investigators interested in determining the underlying causes of drug-induced CTA blockade may choose to employ paradigms similar to the one used here.