Forebrain structures specifically activated by conditioned taste aversion.

Ferry, Barbara; Meurisse, Maryse; Lévy, Frédéric

doi:10.1037/0735-7044.120.4.952

Cited by 38 publications

(24 citation statements)

References 47 publications

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“…Interestingly, consistent with previous studies showing that LiCl injection did not induce the expression of the activation marker c-fos in the GC (16)(17)(18), the malaise itself does not induce significant changes in the correlations between saccharin and quinine patterns (P CS-Ctrl/US-Ctrl ϭ In the following test days (TD1 and TD2), a preference test for distilled water (Wat.) over saccharin (Sac.)…”

Section: Resultssupporting

confidence: 75%

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Internal body state influences topographical plasticity of sensory representations in the rat gustatory cortex

Accolla

Carleton²

2008

Proc. Natl. Acad. Sci. U.S.A.

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Primary sensory cortices are remarkably organized in spatial maps according to specific sensory features of the stimuli. These cortical maps can undergo plastic rearrangements after changes in afferent (''bottom-up'') sensory inputs such as peripheral lesions or passive sensory experience. However, much less is known about the influence of ''top-down'' factors on cortical plasticity. Here, we studied the effect of a visceral malaise on taste representations in the gustatory cortex (GC). Using in vivo optical imaging, we showed that inducing conditioned taste aversion (CTA) to a sweet and pleasant stimulus induced plastic rearrangement of its cortical representation, becoming more similar to a bitter and unpleasant taste representation. Using a behavior task, we showed that changes in hedonic perception are directly related to the maps plasticity in the GC. Indeed imaging the animals after CTA extinction indicated that sweet and bitter representations were dissimilar. In conclusion, we showed that an internal state of malaise induces plastic reshaping in the GC associated to behavioral shift of the stimulus hedonic value. We propose that the GC not only encodes taste modality, intensity, and memory but extends its integrative properties to process also the stimulus hedonic value.chemical senses ͉ map plasticity ͉ taste coding

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Section: Resultssupporting

confidence: 75%

“…We took advantage of the unique features of the central taste system where changes in internal body states, such as satiety (20) or visceral malaise (16,19) have a direct influence on primary GC neuronal responses.…”

Section: Discussionmentioning

confidence: 99%

Internal body state influences topographical plasticity of sensory representations in the rat gustatory cortex

Accolla

Carleton²

2008

Proc. Natl. Acad. Sci. U.S.A.

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“…In fact, the analysis of c-Fos IR in the CNA revealed that the density of Fos-positive nuclear profiles increases following the LiCl-only injection, but the magnitude of this increase is greater when the blockade of the NOP occurs. This is in concert with previous studies showing that LiCl elevates c-Fos IR in the CNA (43), and the c-Fos response depends on the strength of the aversive stimulus (11). Additionally, the level of c-Fos IR in the amygdala is memorydependent following the induction of a CTA (43).…”

Section: Discussionsupporting

confidence: 72%

Central nociceptin/orphanin FQ system elevates food consumption by both increasing energy intake and reducing aversive responsiveness

Olszewski

Grace²,

Fard

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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/orphanin FQ (N/OFQ), the nociceptin opioid peptide (NOP) receptor ligand, increases feeding when injected centrally. Initial data suggest that N/OFQ blocks the development of a conditioned taste aversion (CTA). The current project further characterized the involvement of N/OFQ in the regulation of hunger vs. aversive responses in rats by employing behavioral, immunohistochemical, and real-time PCR methodology. We determined that the same low dose of the NOP antagonist [Nphe 1 ]N/OFQ(1-13)NH2 delivered via the lateral ventricle diminishes both N/OFQand deprivation-induced feeding. This anorexigenic effect did not stem from aversive consequences, as the antagonist did not cause the development of a CTA. When [Nphe 1 ]N/OFQ(1-13)NH2 was administered with LiCl, it moderately delayed extinction of the LiClinduced CTA. Injection of LiCl ϩ antagonist compared with LiCl alone generated an increase in c-Fos immunoreactivity in the central nucleus of the amygdala. The antagonist alone elevated Fos immunoreactivity in the paraventricular nucleus of the hypothalamus, nucleus of the solitary tract, and central nucleus of the amygdala. Hypothalamic NOP mRNA levels were decreased during energy intake restriction induced by aversion, as well as in non-CTA rats food-restricted to match CTA-reduced consumption. Brain stem NOP was upregulated only in aversion. Prepro-N/OFQ mRNA showed a trend toward upregulation in restricted rats (P ϭ 0.068). We conclude that the N/OFQ system promotes feeding by affecting the need to replenish lacking calories and by reducing aversive responsiveness. It may belong to mechanisms that shift a balance between the drive to ingest energy and avoidance of potentially tainted food. food intake; conditioning; hypothalamus; brain stem; amygdala; lithium chloride; NOP receptor; ORL1 NOCICEPTIN/ORPHANIN FQ (N/OFQ) is a 17-amino acid endogenous agonist of the opioid-like G protein-coupled receptor ORL1, currently referred to as the nociceptin opioid peptide (NOP) receptor (20,32). N/OFQ and the NOP exhibit a high degree of structural homology to dynorphin and the -opioid receptor, respectively (3, 9). Regardless of this similarity, N/OFQ does not activate opioid receptors, nor does the NOP bind classical opioid receptor ligands (36). The N/OFQ system has been implicated in several physiological and behavioral functions, including regulation of water-electrolyte balance (16), pain perception (5), locomotion (10), sexual behavior (37), and memory and learning (35).The high level of homology between N/OFQ and opioids prompted the following question: Does N/OFQ, similar to opioids (23), elicit hyperphagia? Pomonis et al. (29) reported that lateral ventricular (LV) administration of this peptide moderately increases chow intake; in subsequent studies, mild overeating was also observed following site-specific, but not peripheral, injections of N/OFQ (28, 38). Unlike classical opioids, N/OFQ primarily affects eating for energy, not for palatability (22,28).Aside from N/OFQ's involvement in the control of hunge...

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“…Two hours later rats received ip injections of either 0.4 M LiCl or physiological saline at 1.0 ml/100 g. The pattern and magnitude of c-Fos expression has been found to be the same following administration of 0.15 M or 0.4 M NaCl (Ferreira, Ferry, Meurisse, & Lévy, 2006). Therefore, 0.15 M saline was used in the control condition of the present study.…”

Section: Methodsmentioning

confidence: 99%

“…The remaining structures innervated by the PBN (GT, BNST, IC) have been examined to a much lesser degree typically in experiments in which lithium was administered as a control condition (e.g., LiCl-only) and therefore was not the focus of the investigation. These studies suggest (1) little involvement of the IC (Billig, Yates, & Rinaman, 2001;Ferreira, Ferry, Meurisse, & Lévy, 2006) and (2) that the medial BNST may express c-Fos following lithium treatment in the ferret (Billig et al, 2001); to our knowledge the GT has not been investigated. The purpose of this study is to confirm these prior findings and to explore additional structures implicated in LiCl-induced viscerosensory information processing.…”

Section: Introductionmentioning

confidence: 97%

C-fos expression in the rat brain following lithium chloride-induced illness

2007

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The present study examined c-Fos expression in selected brain areas consequent to administration of lithium chloride, the typical illness-inducing agent used in laboratory studies of conditioned taste aversion. The results replicated previous findings of significant c-Fos expression in the parabrachial nucleus, the central nucleus of the amygdala and the basolateral amygdala. New findings indicate significant lithium-induced c-Fos in the gustatory region of the thalamus and the bed nucleus of the stria terminalis but not in the insular cortex. The results are discussed with respect to the neural substrates of conditioned taste aversion.

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Forebrain structures specifically activated by conditioned taste aversion.

Cited by 38 publications

References 47 publications

Internal body state influences topographical plasticity of sensory representations in the rat gustatory cortex

Internal body state influences topographical plasticity of sensory representations in the rat gustatory cortex

Central nociceptin/orphanin FQ system elevates food consumption by both increasing energy intake and reducing aversive responsiveness

C-fos expression in the rat brain following lithium chloride-induced illness

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