Jian-You Lin

Conditioned taste aversion and latent inhibition following extensive taste preexposure in rats with insular cortex lesions

Lesions of the insular cortex (IC) attenuate acquisition of conditioned taste aversions (CTAs). We have suggested that this impairment is the expected consequence of a failure of IC-lesioned (ICX) rats to recognize unfamiliar taste stimuli as novel. That is, ICX rats treat novel taste stimuli as if they are familiar and as a result show a latent inhibition-like retardation of learning. This account anticipates that ICX rats should acquire CTAs at the same slow rate as normal rats that are familiar with the taste stimulus. The present experiment confirmed this hypothesis in a design that compared CTA acquisition in normal and ICX rats following either extensive taste familiarization or no taste familiarization prior to conditioning.

Taste, olfactory and trigeminal neophobia in rats with forebrain lesions

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.

Taste neophobia and palatability: The pleasure of drinking

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.

Conditioned taste aversion, drugs of abuse and palatability.

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.

Reduced palatability in drug-induced taste aversion: II. Aversive and rewarding unconditioned stimuli.

Drugs of abuse are known to reduce intake of a taste conditioned stimulus (conditional stimulus, CS), a behavioral response sometimes seen as paradoxical because the same drugs also serve as rewards in other behavioral procedures. In the present study we compared patterns of intake and palatability (assessed using microstructural analysis of licking) for a standard saccharin CS paired with the following: lithium chloride, morphine, amphetamine, or sucrose. We found that morphine and amphetamine, like lithium-induced illness, each suppressed CS intake and caused a reduction in saccharin palatability. Sucrose, a rewarding stimulus, did not reduce the palatability of the saccharin CS. We interpret these finds as evidence that drugs of abuse induce conditioned taste aversions.

Reduced Palatability in Drug-Induced Taste Aversion: I. Variations in the Initial Value of the Conditioned Stimulus

Like illness-inducing agents (e.g., lithium chloride), drugs of abuse also suppress intake of a taste solution. To explore the nature of this drug-induced intake reduction, in the current study three aqueous stimuli with different initial values served as the conditioned stimuli (CSs) that were paired with a standard dose of amphetamine in a voluntary intake procedure and lick patterns were analyzed. Consistent with earlier studies, amphetamine significantly reduced intake of all three CSs (quinine, sodium chloride, and orange odor). In contrast to studies that analyze orofacial responses, we found that lick cluster size was significantly lowered by amphetamine, indicating that the psychoactive drug induced a conditioned reduction in taste palatability.

Taste neophobia and c-Fos expression in the rat brain.

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.

Insular Cortex and Consummatory Successive Negative Contrast in the Rat

Rats that are expecting a high value reward (e.g., 1.0 M sucrose) show an exaggerated underresponding when they are instead given a low value reward (e.g., 0.15% saccharin), an effect termed successive negative contrast (SNC). In the present experiment, insular cortex-lesioned (ICX) rats showed normal responsivity to sucrose and saccharin prior to the reward downshift. However, when switched from sucrose to saccharin during the postshift trials these rats displayed no evidence of SNC. Indeed, over the downshift trials these ICX rats consistently drank more saccharin than the ICX rats maintained on saccharin throughout the experiment. Potential interpretations are discussed including a lesion-induced impairment in the ability to accurately recognize the novelty of the postshift saccharin stimulus.

Conditioned taste aversions: From poisons to pain to drugs of abuse

Learning what to eat and what not to eat is fundamental to our well-being, quality of life, and survival. In particular, the acquisition of conditioned taste aversions (CTAs) protects all animals (including humans) against ingesting foods that contain poisons or toxins. Counterintuitively, CTAs can also develop in situations in which we know with absolute certainty that the food did not cause the subsequent aversive systemic effect. Recent nonhuman animal research, analyzing palatability shifts, has indicated that a wider range of stimuli than has been traditionally acknowledged can induce CTAs. This article integrates these new findings with a reappraisal of some known characteristics of CTA and presents a novel conceptual analysis that is broader and more comprehensive than previous accounts of CTA learning.

Reduced palatability in pain-induced conditioned taste aversions

The current study investigated whether internal pain-inducing agents can modulate palatability of a tastant in the same way as illness-inducing agents (e.g., lithium chloride). Similar to traditional conditioned taste aversion (CTA) experiments, during conditioning the rats were exposed to a saccharin solution followed by intraperitoneal injections of either gallamine (Experiment 1) or hypertonic sodium chloride (NaCl; Experiments 1 and 2). In addition to the total amount consumed, the time of each lick was recorded for lick pattern analysis. The results showed that both gallamine and hypertonic NaCl caused suppression in saccharin intake. Importantly, both lick cluster size and initial lick rate (the measures of taste palatability) were reduced as well. This pattern of results suggests that these pain-inducing agents reduce the hedonic value of the associated tastant and thus CTA is acquired. The current finding serves as evidence supporting the view that CTA is a broadly tuned mechanism that can be triggered by changes in internal body states following consummatory experience.