Cholinergic dependence of taste memory formation: Evidence of two distinct processes

Perirhinal Cortex Muscarinic Receptor Blockade Impairs Taste Recognition Memory Formation

“…It should be noted that scopolamine prevented attenuation of neophobia even when it was administered after taste stimulation, which provides support to the idea that activation of cortical muscarinic receptors is necessary to consolidate this memory. Importantly, the same treatment has no noticeable effect on consolidation of CTA, which indicates that attenuation of neophobia and conditioned taste aversion seems to rely on different cortical processes once the rat has sampled the taste and formed a representation of it (Gutierrez et al 2003b). …”

“…However, animals overcome this neophobia, displaying higher saccharin consumption on subsequent presentations, which reflects a learning process (Gutierrez et al 2003b). Therefore, we used the neophobic response as a novelty detection index and the subsequent attenuation of neophobia (AN) as a recognition memory index, based on the supposition that to display AN rats must recognize the taste as familiar and recall that the solution is safe to drink (Gutierrez et al 2003b).…”

“…Thus, Tassoni et al (2000), using a sodium channel blocker (TTX), reported that temporal inactivation of the perirhinal cortex when rats drink a novel taste solution impairs CTA, but the impairment was not observed when inactivation was induced between taste exposure and induction of malaise (association phase) or before the retrieval test. These results indicate that the perirhinal cortex is involved in the formation of the taste memory trace (TMT; for definition, see Gutierrez et al 2003b), but not in the association or retrieval of learned taste aversion.…”

“…It has been previously demonstrated that scopolamine impairs specifically the formation of the TMT when it is injected in the insular cortex (Naor and Dudai 1996;Ferreira et al 2002;Gutierrez et al 2003b). In addition, NMDA and AMPA receptor blockers were also applied because previous reports indicate that glutamatergic activity is required in the insular cortex for CTA long-term memory but not for taste memory trace formation (Ferreira et al 2002;Gutierrez et al 2003a,b).…”

The Insular Cortex and the Amygdala: Shared Functions and Interactions

“…IC lesions appear to produce no effects on animals' capacity to attain taste familiarity [151], but several reports document a role for the IC in taste familiarity learning as a result of pharmacological manipulations [153,154], showing that taste familiarity requires cholinergic activity in the IC [155,156] but that it is independent of NMDA and AMPA channel activity [157][158][159][160]. Perhaps this dichotomy can be explained either by compensation from other areas after IC lesions or, given the role of neophobia discussed above, it is possible that IC output per se may modulate familiarity.…”