Abstract
Latent inhibition (LI) is a term that describes the retardation of learning of a stimulusoutcome pailing that occurs when conditioning is preceded by nonreinforced stimulus exposures. LI can be shown in a variety of animal learning paradigms. Research on the role of the hippocampus in LI has resulted in incongruent conclusions. However, when experimental variability is taken into account, the majority of studies suggest that hippocampal lesions disrupt LI. In contrast, two experiments using the conditioned taste aversion (CTA) paradigm show that electrolytic and excitotoxic hippocampal lesions lead to enhanced LI. In this study, the role of the hippocampus in LI of CTA was examined via reversible muscimol inactivation of the dorsal hippocampus (dHIPP) rather than a pern1anent lesion. Using a within-subjects design, each animal was preexposed to a fixed amount of one tastant and conditioned to it simultaneously with a novel tastant. LI was evaluated in each animal as decreased conditioning to the preexposed versus the novel tastant. Two near-significant results were observed: Bilateral dHIPP infusions of muscimol during preexposure and conditioning led to both an LI enhancement and an increase in CT A to the novel tastant. These results reflect one of two possible phenomena, either hippocampal inactivation facilitates CTA or enhances both LI and CTA simultaneously. As previous research shows that CTA learning itself is not altered by lesions, these results suggest that hippocampal inactivation affects learning differently than a permanent lesion does. A possible mechanism for this effect is discussed.