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.

Accumbens and amygdala in taste recognition memory: The role of d1 dopamine receptors.

The attenuation of taste neophobia (AN) is a good model for studying the structural and neurochemical mechanisms of the emotional component of memory because taste recognition memory exhibits the unique feature of being necessarily linked to hedonic properties. Whilst novel tastes elicit cautious neophobic responses, taste exposures which are not followed by aversive consequences attenuate neophobia as the taste becomes safe and palatable. Given the involvement of the nucleus accumbens in reward and of the amygdala in emotional memories, we applied c-Fos immunohistochemistry as an index of neural activity in Wistar rats that were exposed to a vinegar solution for one, two or six days.

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.

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.