Research reportDifferential contribution of perirhinal cortex and hippocampus to taste neophobia: Effect of neurotoxic lesions

- Perirhinal lesions impair neophobic response to novel 0.3% and 0.5% saccharin solution.
- Perirhinal lesions do not affect neophobic response to novel 0.7% saccharin solution.
- Hippocampus lesions before novel saccharin do not impair neophobic response.
- Hippocampus lesions 24 h after saccharin do not affect consolidation of taste memory.

Although the perirhinal cortex (Prh) has been extensively related to recognition memory, little is known about its specific role in taste memories. The main aim of the present series was therefore to examine the effect of neurotoxic lesions of the Prh on taste neophobia, a phenomenon consisting of a low intake of a novel food until its postingestive consequences are determined. The results showed that Prh-lesioned rats consumed significantly more novel saccharin in trial 1 than control subjects when a saccharin solution of 0.3% (expt. 1a) and 0.5% (expt. 1b) was presented. However, when the saccharin concentration was high and qualitatively more aversive, Prh lesions did not affect the neophobic response (0.7%, expt. 1c) and the lesioned and control animals consumed a similar amount of the fluid during the first and subsequent test trials. In all three experiments, Prh-lesioned and control rats showed a comparable intake at asymptote. Experiment 2 and 3 showed that neurotoxic lesions to the dorsal hippocampus prior to or 24 h after the intake of the novel taste (0.3% saccharin) had no effect on the initial occurrence of the neophobic response or on the consolidation of safe taste memory, respectively. These findings support a dissociation of functions between the Prh and the hippocampus in taste neophobia. Also, the data suggests that the Prh plays an essential role in detecting the novelty of the new tastant.