Glucocorticoid and Other Hormonal Substrates of Conditioned Taste Aversion

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Abstract
Results of research reported in this paper show that lithium chloride (LiCl) injection causes a marked and prolonged elevation of adrenocorticotropic hormone (ACTH) and corticosterone. Peak elevations occur within 30 min after injection and continue for 60 to 120 min depending upon the molarity of the LiCl solution. CS preexposures do not alter the pituitary-adrenal response to LiCl. Although this response occurs, evidence argues that pituitary-adrenal activity is neither a sufficient nor essential condition for CTA to occur. It is possible that this prolonged ACTH secretion, which would be essential to maintain corticosterone levels elevated for one to two hours, is acting as a component of the unconditioned response associated with LiCl injections. Under certain types of extinction (forced extinction) the P-A system is activated. Thus, when an animal drinks an aversive solution following deprivation, intake of the solution causes a conditioned elevation of plasma corticosterone. Two measures of CTA, behavioral and hormonal, do not always coincide with one another. Preexposure to the CS alters both behavioral and corticosterone indices of CTA. These two systems will show either a coupling (e.g., parallel change) or a dissociation depending on the number of preexposures prior to conditioning. Manipulating the hormones associated with the pituitary-adrenal system also affects the acquisition of CTA and influences extinction. Thus, if one pretests with dexamethasone phosphate (DEX) prior to the administration of LiCl, CTA is attenuated. It would appear that ACTH is involved in the acquisition of CTA since a central block of ACTH also affects the magnitude of the aversion. If ACTH is injected during recovery, animals show a prolonged suppression of drinking. These data appear to be best explained using a memory-retrieval model. The manipulation of hormones and their effects on CTA appear to follow the effects observed endogenously. Thus, ACTH administered to rats during the conditioning phase does not appear to have any effect upon the learning of the aversion. Since LiCl markedly elevates ACTH, as indicated by prolonged elevations of corticosterone, the additional ACTH given exogenously at the time of conditioning does not appear to add to the effects already attributable to endogenous ACTH. Conversely, DEX given during recovery appears to have no effect upon the recovery function. Because endogenous levels of ACTH are already low during the free extinction procedure, DEX treatment does not appear to further reduce ACTH and has no effect upon recovery.(ABSTRACT TRUNCATED AT 400 WORDS)