Involvement of gustatory neocortex in the learning of taste aversions☆
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Cited by (96)
3.14 - Taste Pathways, Representation and Processing in the Brain
2020, The Senses: A Comprehensive Reference: Volume 1-7, Second EditionGustatory insular cortex, aversive taste memory and taste neophobia
2015, Neurobiology of Learning and MemoryCB<inf>1</inf> receptor antagonism in the granular insular cortex or somatosensory area facilitates consolidation of object recognition memory
2014, Neuroscience LettersCitation Excerpt :Specifically, the insular cortex (IC), which is extensively connected via afferent and efferent pathways to medial temporal structures [17], appears to be involved in recognition memory in rats [16,18]. Historically associated with taste learning and disgust [19,20], the IC also appears to be involved in the consolidation of object information required for recognition memory [16,18]. The IC is subdivided, based on its degree of granularity, into the posterior or granular IC, and the anterior or agranular IC [21].
The forgotten insular cortex: Its role on recognition memory formation
2014, Neurobiology of Learning and MemoryCitation Excerpt :James McGaugh, based on many years of research, has postulated that amygdala activation enables memory consolidation in other parts of the brain, like the cortex or hippocampus, and that this influence could be mainly through the modulation of the noradrenergic system in the amygdala (McGaugh, 2004; McIntyre, Power, Roozendaal, & McGaugh, 2003). The first experiments focusing on the cognitive processing related with the IC started at the beginning of the ‘70s, mainly with aversive taste memory formation (Braun, Kiefer, & Ouellet, 1981; Braun, Slick, & Lorden, 1972). The amygdala and the IC are reciprocally interconnected, and both areas are necessary for CTA consolidation (Gallo, Roldan, & Bures, 1992; Ishikawa et al., 1999; Roldan & Bures, 1994).
Conditioned flavor avoidance and conditioned gaping: Rat models of conditioned nausea
2014, European Journal of PharmacologyCitation Excerpt :The literature on the effect of neurotoxin-induced or electrolytic lesions of the IC on the establishment of LiCl-induced flavor avoidance in rats is mixed. Damage to the gustatory area of input, the anterior dysganular region (gustatory cortex), has been reported to attenuate (but not eliminate) LiCl-induced flavor avoidance (e.g., Braun et al., 1972; Hankins et al., 1974; Lasiter, 1982; Lasiter and Glanzman, 1985; Dunn and Everitt, 1988; Bermúdez-Rattoni and McGaugh, 1991; Nerad et al., 1996; Roman and Reilly, 2007), but damage to the visceral area of input, the posterior granular region (visceral cortex) has been reported to be ineffective in attenuation of LiCl-induced flavor avoidance (Mackey et al., 1986; Nerad et al., 1996). On the other hand, in the single study that has evaluated the role of the IC in conditioned gaping in rats, Kiefer and Orr (1992) showed that rats with complete bilateral ablation of the IC learned to avoid drinking sucrose and salt that was paired with LiCl (albeit at a slower rate than controls), but they failed to display gaping reactions to the tastes.
Metabolic regulation of brain response to food cues
2013, Current BiologyCitation Excerpt :However, a significant correlation was observed between response in the anterior insular cortex to the CS+ flavor versus the control flavor and the magnitude of hedonic conditioning for the CS+ beverage (liking ratings recorded during post- minus preconditioning sessions) Figure 2B. This raises the possibility that postoral signals act upon insular circuits to change flavor liking, a proposal consistent with the known role of this region of insular cortex in oral sensory, homeostatic representation [19], and conditioned taste-aversion learning [20]. However, we also note that these effects might have been accounted for by exposure alone, independently of conditioning effects per se.
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Supported by NIH grant NS08658. We thank Geoffrey Nowlis and Edwin Rubel for reviewing the preliminary manuscript, and Harris McIntosh Jr. for technical assistance.