Morphine-induced Suppression of Conditioned Stimulus Intake: Effects of Stimulus Type and Insular Cortex Lesions

Intake of an unconditionally preferred taste stimulus (e.g., saccharin) is reduced by contingent administration of a drug of abuse (e.g., morphine). We examined the influence of insular cortex (IC) lesions on morphine-induced suppression of an olfactory cue and two taste stimuli with different levels of perceived innate reward value. Two major findings emerged from this study. First, morphine suppressed intake of an aqueous odor as well as each taste stimulus in neurologically intact rats. Second, IC lesions disrupted morphine-induced suppression of the taste stimuli but not the aqueous odor cue. These results indicate that the perceived innate reward value of the CS is not a factor that governs drug-induced intake suppression

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 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-Potentiated Odor Aversion Learning in Rats with Lesions of the Insular Cortex

The current study assessed the influence of excitotoxic lesions of the insular cortex (IC) on tastepotentiated odor aversion (TPOA) learning. Water-deprived rats initially received a single odortoxicosis or odor/taste-toxicosis pairing and were subsequently tested, in separate trials, with the odor and the taste stimulus. Indicating TPOA, neurologically intact rats conditioned with the odor/taste compound stimulus acquired significantly stronger odor aversions than normal rats conditioned with the odor stimulus. IC lesions disrupted TPOA, conditioned taste aversion and taste neophobia. The finding that taste did not potentiate odor aversion learning in the IC lesioned rats provides support for the “within-compound association” analysis but is inconsistent with the “sensory and-gate” account of TPOA learning

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

Basolateral Amygdala and Morphine-Induced Taste Avoidance in the Rat

The present experiment examined the influence of excitotoxic lesions of the basolateral amygdala (BLA) on morphine-induced saccharin avoidance. Neurologically intact subjects rapidly learned to avoid drinking the taste conditioned stimulus (CS), an effect that was sustained throughout the experiment. Although the BLA-lesioned (BLAX) rats showed CS avoidance over the first few trials, the effect was not sustained. That is, by the end of the experiment, the BLAX rats were drinking the same amount of saccharin after seven saccharin-morphine trials as they did on the first trial (i.e., prior to the morphine injections). Potential interpretations of the results are discussed including a disruption of the mechanism that governs drug-induced taste avoidance in normal subjects and the more rapid development of tolerance in BLAX rats

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

Entanglement and quantum phase transition in the extended Hubbard model

We study quantum entanglement in one-dimensional correlated fermionic system. Our results show, for the first time, that entanglement can be used to identify quantum phase transitions in fermionic systems.Comment: 5 pages, 4 figure