Neural substrates for conditioned taste aversion in the rat

Yamamoto, Takashi; Shimura, Tsuyoshi; Sako, Noritaka; Yasoshima, Yasunobu; Sakai, Nobuyuki

doi:10.1016/0166-4328(94)90097-3

Cited by 271 publications

(157 citation statements)

References 144 publications

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“…10. The association between CS and US is likely to happen at the brainstem level, in the parabrachial nucleus, the US-relevant (visceral) information is transmitted to the amygdala and then to the cortex via glutamatergic projections (30), whereas taste-related information follows a classical brainstemthalamic pathway (31).…”

Section: Discussionmentioning

confidence: 99%

“…An efficient paradigm of conditioned learning experience is given by conditioned taste aversion (CTA), where a subject learns to avoid a taste stimulus (CS) paired with visceral malaise (US) (9), even after a single learning procedure (10). The primary gustatory cortex (GC) is an important part of the brain circuitry involved in CTA acquisition, long-term retention, and extinction (10)(11)(12). The GC therefore constitutes an ideal region to investigate sensory maps plasticity after conditioned learning.…”

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confidence: 99%

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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: Discussionmentioning

confidence: 99%

mentioning

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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“…Forebrain areas are required for learning a flavour aversion in rat because decerebrate animals fail to show a conditioned response (Grill and Norgren, 1978). However, although specific ablation of forebrain regions block CFA in the rat it is difficult to determine whether these brain regions are important for the experience of malaise, and perhaps nausea in humans, or are involved in memory and learning processes of CFA (for review see Yamamoto et al, 1994). Currently there are no published reports on the effects of brain or peripheral nerve lesions on pica.…”

Section: Neural Circuitry For Nauseamentioning

confidence: 99%

Signals for nausea and emesis: Implications for models of upper gastrointestinal diseases

Andrews

Horn

2006

Autonomic Neuroscience

214

200

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Nausea and vomiting are amongst the most common symptoms encountered in medicine as either symptoms of diseases or side effects of treatments. In a more biological setting they are also important components of an organism's defences against ingested toxins. Identification of treatments for nausea and vomiting and reduction of emetic liability of new therapies has largely relied on the use of animal models, and although such models have proven invaluable in identification of the anti-emetic effects of both 5-hydroxytryptamine3 and neurokinin1 receptor antagonists selection of appropriate models is still a matter of debate. The present paper focuses on a number of controversial issues and gaps in our knowledge in the study of the physiology of nausea and vomiting including: The choice of species for the study of emesis and the underlying behavioural (e.g. neophobia), anatomical (e.g. elongated, narrow abdominal oesophagus with reduced ability to shorten) and physiological (e.g. brainstem circuitry) mechanisms that explain the lack of a vomiting reflex in certain species (e.g. rats); The choice of response to measure (emesis[retching and vomiting], conditioned flavour avoidance or aversion, ingestion of clay [pica], plasma hormone levels[e.g. vasopressin], gastric dysrhythmias) and the relationship of these responses to those observed in humans and especially to the sensation of nausea; The stimulus coding of nausea and emesis by abdominal visceral afferents and especially the vagus-how do the afferents encode information for normal postprandial sensations, nausea and finally vomiting?; Understanding the central processing of signals for nausea and vomiting is particularly problematic in the light of observations that vomiting is more readily amenable to pharmacological treatment than is nausea, despite the assumption that nausea represents "low" intensity activation of pathways that can evoke vomiting when stimulated more intensely.

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“…Nevertheless, CTA memory can be extinguished following retrieval in the absence of reinforcer. Both acquisition and extinction of CTA are subserved by the amygdala (Bahar et al, 2004;Yamamoto et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

NMDA Partial Agonist Reverses Blocking of Extinction of Aversive Memory by GABAA Agonist in the Amygdala

Akirav

2006

Neuropsychopharmacol

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The ability to extinguish aversive memories is of significant clinical interest. The amygdala plays an important role in emotional conditioning and its experimental extinction. It has been suggested that g-aminobutyric acid (GABA) agonists retard extinction and that consolidation of extinction involves N-methyl-D-aspartate receptor (NMDAR)-mediated plasticity. The aim was to further explore the interaction between GABA and NMDA in the amygdala in consolidation of experimental extinction in the rat. To that end conditioned taste aversion (CTA) was used. In CTA, the amygdala has been reported to subserve both acquisition and extinction. The GABA A receptor agonist, muscimol, administered into the amygdala immediately after the first extinction session, caused lasting disruption of extinction of CTA for at least 2 weeks. However, the administration of GABA A receptor antagonists had no effect on extinction kinetics. Microinfusing the partial NMDA agonist D-cycloserine together with or after muscimol infusion reversed the blocking effects of muscimol. These findings could bear relevance to the potential involvement of extinction abnormalities in behavioral disorders, and their amelioration.

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Neural substrates for conditioned taste aversion in the rat

Cited by 271 publications

References 144 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

Signals for nausea and emesis: Implications for models of upper gastrointestinal diseases

NMDA Partial Agonist Reverses Blocking of Extinction of Aversive Memory by GABAA Agonist in the Amygdala

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