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Literature DB >> 19170445

Insular cortex lesions and morphine-induced suppression of conditioned stimulus intake in the rat.

Abstract

The present experiment examined the influence of insular cortex (IC) lesions on the intake of a taste stimulus in a consummatory procedure that used morphine as the unconditioned stimulus. In normal rats, morphine caused a rapid reduction in saccharin intake when the taste was novel but not when it was familiar. Irrespective of stimulus novelty, morphine had little influence on the saccharin consumption of IC-lesioned rats. The results are discussed in terms of a lesion-induced disruption of (i) a reward comparison mechanism and (ii) the perception of taste novelty. (c) 2009 APA, all rights reserved.

Entities: Chemical Disease Species

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Year: 2009 PMID： 19170445 PMCID： PMC2709771 DOI： 10.1037/a0014308

Source DB: PubMed Journal: Behav Neurosci ISSN： 0735-7044 Impact factor: 1.912

26 in total

1. Progressive ratio performance in rats with gustatory thalamus lesions.

Authors: S Reilly; R Trifunovic
Journal: Behav Neurosci Date: 1999-10 Impact factor: 1.912

2. Gustatory thalamus lesions eliminate successive negative contrast in rats.

Authors: S Reilly; R Trifunovic
Journal: Behav Neurosci Date: 1999-12 Impact factor: 1.912

3. Projections of thalamic gustatory and lingual areas in the rat.

Authors: R Norgren; G Wolf
Journal: Brain Res Date: 1975-07-04 Impact factor: 3.252

4. Gustatory thalamus lesions eliminate successive negative contrast in rats: evidence against a memory deficit.

Authors: Steve Reilly; Radmila Trifunovic
Journal: Behav Neurosci Date: 2003-06 Impact factor: 1.912

5. Excitotoxic lesions of the gustatory thalamus spare simultaneous contrast effects but eliminate anticipatory negative contrast: evidence against a memory deficit.

Authors: Steve Reilly; Marina Bornovalova; Radmila Trifunovic
Journal: Behav Neurosci Date: 2004-04 Impact factor: 1.912

6. Insular cortex lesions alter conditioned taste avoidance in rats differentially when using two methods of sucrose delivery.

Authors: Nadine Fresquet; Marie-Josée Angst; Guy Sandner
Journal: Behav Brain Res Date: 2004-08-31 Impact factor: 3.332

7. Bilateral lesions of the gustatory thalamus disrupt morphine- but not LiCl-induced intake suppression in rats: evidence against the conditioned taste aversion hypothesis.

Authors: P S Grigson; P Lyuboslavsky; D Tanase
Journal: Brain Res Date: 2000-03-10 Impact factor: 3.252

8. Absence of differential associative responses to novel and familiar taste stimuli in rats lacking gustatory neocortex.

Authors: S W Kiefer; J J Braun
Journal: J Comp Physiol Psychol Date: 1977-06

Insular cortex lesions and morphine-induced suppression of conditioned stimulus intake in the rat.

1. Progressive ratio performance in rats with gustatory thalamus lesions.

2. Gustatory thalamus lesions eliminate successive negative contrast in rats.

3. Projections of thalamic gustatory and lingual areas in the rat.

4. Gustatory thalamus lesions eliminate successive negative contrast in rats: evidence against a memory deficit.

5. Excitotoxic lesions of the gustatory thalamus spare simultaneous contrast effects but eliminate anticipatory negative contrast: evidence against a memory deficit.

6. Insular cortex lesions alter conditioned taste avoidance in rats differentially when using two methods of sucrose delivery.

7. Bilateral lesions of the gustatory thalamus disrupt morphine- but not LiCl-induced intake suppression in rats: evidence against the conditioned taste aversion hypothesis.

8. Absence of differential associative responses to novel and familiar taste stimuli in rats lacking gustatory neocortex.

9. Involvement of gustatory neocortex in the learning of taste aversions.

10. Projections of thalamic and cortical gustatory areas in the rat.

1. Role of the insular cortex in morphine-induced conditioned taste avoidance.

2. Basolateral amygdala and morphine-induced taste avoidance in the rat.

3. Morphine-induced suppression of conditioned stimulus intake: effects of stimulus type and insular cortex lesions.