The present study was designed to examine whether lesions of the insular cortex (IC; Experiment 1), the basolateral amygdala (BLA) or medial amygdala (MeA; Experiment 2) influence the neophobic reactions to orally consumed liquid stimuli. Three different types of stimuli were used: taste (0.5% saccharin), olfactory (0.1% amyl acetate), and trigeminal (0.01 mM capsaicin). Rats with IC, BLA and MeA lesions showed normal responses to the olfactory and trigeminal stimuli. Each type of lesion, however, disrupted the initial occurrence of neophobia to the taste stimulus. The significance of these findings to conditioned taste aversion is discussed.

LIN, J.-Y., J. Arthurs and S. Reilly. Conditioned taste aversion: Palatability and drugs of abuse. NEUROSCI BIOBEHAV REV XX(x) XXX-XXX, 2014. – We consider conditioned taste aversion to involve a learned reduction in the palatability of a taste (and hence in amount consumed) based on the association that develops when a taste experience is followed by gastrointestinal malaise. The present article evaluates the well-established finding that drugs of abuse, at doses that are otherwise considered rewarding and self-administered, cause intake suppression. Our recent work using lick pattern analysis shows that drugs of abuse also cause a palatability downshift and, therefore, support conditioned taste aversion learning.

A great deal is known about the broad coding and neural ensemble dynamics characterizing forebrain taste processing in awake rats, and about the relationship between these firing rate dynamics and behavior. With regard to mice, in contrast, data concerning cortical taste coding are few, inconclusive, and largely restricted to imaging, which lacks the temporal sensitivity necessary for evaluation of fast response dynamics. Here we have recorded the spiking activity of ensembles of gustatory cortical (GC) single neurons while presenting representatives of the basic taste modalities (sweet, salty, sour and bitter) to awake mice. Our results reveal deep similarities between rat and mouse taste processing. Many recorded murine GC neurons (~66%) responded distinctly to different tastes, and entropy analysis (which measures the breadth of taste coding) further confirmed that the majority of taste neurons in fact responded to 3 or 4 tastes. Temporal coding analyses revealed that single mouse GC neurons sequentially coded taste identity and palatability-the latter responses emerging ~0.5s after the former-a dynamic that population analysis suggested reflects a reliable sequence of network states activated by taste delivery (i.e., ensembles of simultaneously-recorded neurons transitioned suddenly and coherently from coding taste identity to coding taste palatability). All of the above results held across the anterior-posterior and dorsal-ventral axes of GC-neither between-nor within-mouse mapping revealed regions of narrow or temporally simple taste responses. In conclusion, our data indicates that mouse GC, like rat GC, codes multiple aspects of taste in a coarse, time-varying manner.

Taste neophobia refers to a reduction in consumption of a novel taste relative to when it is familiar. To gain more understanding of the neural basis of this phenomenon, the current study examined whether a novel taste (0.5% saccharin) supports a different pattern of c-Fos expression than the same taste when it is familiar. Results revealed that the taste of the novel saccharin solution evoked more Fos immunoreactivity than the familiar taste of saccharin in the basolateral region of the amygdala, central nucleus of the amygdala, gustatory portion of the thalamus, and the gustatory insular cortex. No such differential expression was found in the other examined areas, including the bed nucleus of stria terminalis, medial amygdala, and medial parabrachial nucleus. The present results are discussed with respect to a forebrain taste neophobia system.

Taste neophobia is manifested behaviorally as lower intake of a novel, potentially dangerous tastant relative to the same tastant when it is perceived as safe and familiar. To further characterize this phenomenon, microstructural analysis of lick patterns was used to track the transition from novel to familiar for three tastants: saccharin, quinine and Polycose. The results revealed that in addition to an increase in the amount consumed (for saccharin and quinine but not Polycose), cluster size (an index of palatability) became larger as familiarity with the benign tastants increased. The current finding suggests that the pleasure of drinking increases as the novel, potentially dangerous tastant becomes accepted as safe.