Increased basolateral amygdala metabolic activity during flavor familiarization: an experimental study.

BACKGROUND: Novel flavors elicit a cautious neophobic response which is attenuated as the flavor becomes familiar and safe. The attenuation of neophobia reveals the formation of a safe memory. Previous lesion studies in rats have reported that basolateral amygdala integrity is required for taste neophobia, but not neophobia to flavor, i.e., taste linked to an odorous component. Accordingly, immunohistochemical analyses show that novel tastes induced higher basolateral amygdala activity when compared to familiar ones. However, a different role of basolateral amygdala in flavor attenuation of neophobia is suggested by lesion studies using a vinegar solution. Studies assessing basolateral amygdala activity during flavor attenuation of neophobia are lacking. Thus, we quantified cytochrome oxidase as an index of basolateral amygdala activity along the first and second vinegar exposures in order to assess flavor neophobia and attenuation of neophobia. METHODS: We exposed adult male Wistar rats either once or twice to a 3% cider vinegar solution or water, and compared the basolateral amygdala, piriform cortex and caudate putamen brain metabolic activity using cytochrome c-oxidase histochemistry. RESULTS: We found increased flavor intake and cytochrome c-oxidase histochemistry activity during the second exposure in basolateral amygdala, but not in the piriform cortex and caudate/putamen. CONCLUSIONS: The main finding of the study is that BLA metabolic activity was higher in the group exposed to a familiar vinegar solution than in the groups exposed to either water or a novel vinegar solution.

Increased N-Ethylmaleimide-Sensitive Factor Expression in Amygdala and Perirhinal Cortex during Habituation of Taste Neophobia.

Interactions between GluR2 and N-ethylmaleimide-sensitive factor (NSF) mediate AMPA receptors trafficking. This might be linked with molecular mechanisms related with memory formation. Previous research has shown basolateral amygdala (BLA) dependent activity changes in the perirhinal cortex (PRh) during the formation of taste memory. In the present experiments we investigate both the behavioral performance and the expression profile of NSF and GluR2 genes in several brain areas, including PRh, BLA, and hippocampus. Twenty-one naïve male Wistar rats were exposed to a saccharin solution (0.4%) during the first (novel), the second (Familiar I), and the sixth presentation (Familiar II). Total RNA was extracted and gene expression was measured by quantitative PCR (qPCR) using TaqMan gene expression assays. In addition the expression of the synaptic plasticity related immediate early genes, Homer 1 and Narp, was also assessed. We have found increased expression of NSF gene in BLA and PRh in Group Familiar I in comparison with Familiar II. No changes in the expression of GluR2, Homer 1, and Narp genes were found. The results suggest the relevance of a potential network in the temporal lobe for taste recognition memory and open new possibilities for understanding the molecular mechanisms mediating the impact of sensory experience on brain circuit function.

Basolateral amygdala lesions attenuate safe taste memory-related c-fos expression in the rat perirhinal cortex.

Previous results indicated that damage and pharmacological inactivation of the basolateral amygdala (BLA) interfere with the attenuation of taste neophobia. A similar disruption of safe taste memories formation induced by the inhibition of protein synthesis in the perirhinal cortex (PRh) has been reported. Thus, we have assessed the effect of bilateral BLA neurotoxic lesions on PRh activity after novel and familiar taste exposure. Wistar male rats with NMDA lesions of the BLA and SHAM-operated received two consecutive exposures to a 3% cider vinegar solution. Fos-like immunoreactivity (FLI) was examined as a marker of neuronal activity in PRh. As expected the BLA lesioned group showed no evidence of neophobia attenuation. A similar number of PRh Fos-positive cells were found in SHAM and BLA groups exposed to the novel taste solution. However, the BLA-lesioned group exhibited a lower number of Fos stained cells than the SHAM-lesioned group after being exposed to the familiar taste solution. This supports the notion of BLA and PRh as components of a neural circuit involved in safe taste recognition memory and suggests a role of PRh in various forms of recognition memory.