Abstract
The ability of acetylcholine (ACh) to alter specific functional properties of the cortex endows the cholinergic system with an important modulatory role in memory formation. For example, an increase in ACh release occurs during novel stimulus processing, indicating that ACh activity is critical during early stages of memory processing. During novel taste presentation, there is an increase in ACh release in the insular cortex (IC), a major structure for taste memory recognition. There is extensive evidence implicating the cholinergic efferents of the nucleus basalis magnocellularis (NBM) in cortical activity changes during learning processes, and new evidence suggests that the histaminergic system may interact with the cholinergic system in important ways. However, there is little information as to whether changes in cholinergic activity in the IC are modulated during taste memory formation. Therefore, in the present study, we evaluated the influence of two histamine receptor subtypes, H1 in the NBM and H3 in the IC, on ACh release in the IC during conditioned taste aversion (CTA). Injection of the H3 receptor agonist R-α-methylhistamine (RAMH) into the IC or of the H1 receptor antagonist pyrilamine into the NBM during CTA training impaired subsequent CTA memory, and simultaneously resulted in a reduction of ACh release in the IC. This study demonstrated that basal and cortical cholinergic pathways are finely tuned by histaminergic activity during CTA, since dual actions of histamine receptor subtypes on ACh modulation release each have a significant impact during taste memory formation.
Highlights
The central cholinergic system has long been associated with many aspects of cognitive functioning and there is clear evidence implicating cholinergic neurons in the mediation of learning and memory processes [1,2,3]
The main finding of the present research was the demonstration, in free-moving animals, of neurochemical modulation of ACh release into the insular cortex (IC) being induced by local H3 receptor activation, or H1 receptor inhibition in the nucleus basalis magnocellularis (NBM), during conditioned taste aversion (CTA) acquisition
This study demonstrates that the H1 and H3 receptor subtypes modulate ACh release in distinct ways, and that blocking ACh release into the IC by either manipulation during acquisition impairs subsequent CTA
Summary
The central cholinergic system has long been associated with many aspects of cognitive functioning and there is clear evidence implicating cholinergic neurons in the mediation of learning and memory processes [1,2,3]. The processing of a gustatory stimulus is very complex in and of itself because taste encoding encompasses both the immediate hedonic value of a tastant and one’s overall experience with the perceived flavor. The role of ACh in the recognition of novel taste is well documented [11,12,13,14,15] and consistent with ACh’s established involvement in the encoding of other types of novel-experience memories [4,16,17,18,19]
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