Inactivation of the ventral hippocampus facilitates the attenuation of odor neophobia in rats

Abstract

Food neophobia is a behavior observed in rodents involving reduced consumption of a novel food or drink. In the absence of negative post-ingestive consequences, consumption increases with exposure (attenuation of neophobia), which is seen as an associative safe memory. Olfaction and gustation are sensory modalities essential for the development of a food preference. However, little is known about the neural mechanisms underlying neophobia to a food-related odor stimulus. In the present study, we examined the effect of pharmacological inactivation of the ventral hippocampus (vHPC) on neophobia to orally consumed solutions in rats using muscimol, a gamma aminobutyric acid type A receptor agonist. Two different types of solutions, almond odor (benzaldehyde) and sweet taste (saccharin), were prepared. In the results, microinjections of muscimol into the bilateral vHPC before the first odor and taste exposures did not alter the neophobic reactions of the rats to each stimulus. However, in the second odor, but not taste, exposure, the muscimol-injected rats showed higher consumption in comparison to that observed in the control rats, suggesting that the vHPC inactivation facilitates the attenuation of odor neophobia. On the other hand, intra-vHPC muscimol microinjections after the first odor and taste exposures did not facilitate consumption at the second exposures. These results indicate that neural activations within vHPC during orally consuming a novel odor, but not taste, solution play an inhibitory role in the subsequent attenuation of neophobia.