Effects of lesions of the bed nucleus of the stria terminalis, lateral hypothalamus, or insular cortex on conditioned taste aversion and conditioned odor aversion.

Roman, Christopher T.; Nebieridze, Nino; Sastre, Aristides; Reilly, Steve

doi:10.1037/0735-7044.120.6.1257

Cited by 37 publications

(41 citation statements)

References 89 publications

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“…The absence of increase in oscillatory activity in the granular zone contrary to the agranular zone in response to the first odor presentation confirms the functional heterogeneity of this cortex; however, a major finding is that IC (both aIC and gIC) presented a selective increase of beta oscillatory activity in response to the distal cue when the odor was ingested before intoxication. Although IC is strongly involved in gustatory food aversions (Bermú dez-Rattoni, 2004), its lesion or inactivation has been reported without effect on COA (Kiefer et al, 1982;Roman et al, 2006;Desgranges et al, 2009) and has led to ambiguous results on TPOA (Kiefer et al, 1982;Lasiter et al, 1985;Inui et al, 2006). Methodological differences used in these and our studies could account for the observed differences.…”

Section: An Effective Cs-us Association Duringcontrasting

confidence: 54%

The Way an Odor Is Experienced during Aversive Conditioning Determines the Extent of the Network Recruited during Retrieval: A Multisite Electrophysiological Study in Rats

Chapuis¹,

Garcia²,

Messaoudi³

et al. 2009

J. Neurosci.

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Recent findings have revealed the importance of orthonasal and retronasal olfaction in food memory, especially in conditioned odor aversion (COA); however, little is known about the dynamics of the cerebral circuit involved in the recognition of an odor as a toxic food signal and whether the activated network depends on the way (orthonasal vs retronasal) the odor was first experienced. In this study, we mapped the modulations of odor-induced oscillatory activities through COA learning using multisite recordings of local field potentials in behaving rats. During conditioning, orthonasal odor alone or associated with ingested odor was paired with immediate illness. For all animals, COA retrieval was assessed by orthonasal smelling only. Both types of conditioning induced similarly strong COA. Results pointed out (1) a predictive correlation between the emergence of powerful beta (15-40 Hz) activity and the behavioral expression of COA and (2) a differential network distribution of this beta activity according to the way the animals were exposed to the odor during conditioning. Indeed, for both types of conditioning, the aversive behavior was predicted by the emergence of a strong beta oscillatory activity in response to the odor in the olfactory bulb, piriform cortex, orbitofrontal cortex, and basolateral amygdala. This network was selectively extended to the infralimbic and insular cortices when the odor was ingested during acquisition. These differential networks could participate in different food odor memory; these results are discussed in line with recent behavioral results that indicate that COA can be formed over long odor-illness delays only if the odor is ingested.

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Section: An Effective Cs-us Association Duringcontrasting

confidence: 54%

The Way an Odor Is Experienced during Aversive Conditioning Determines the Extent of the Network Recruited during Retrieval: A Multisite Electrophysiological Study in Rats

Chapuis¹,

Garcia²,

Messaoudi³

et al. 2009

J. Neurosci.

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“…Experiments from our laboratory show that neurotoxic lesions of the insular cortex disrupt the acquisition of conditioned taste aversions (CTAs), particularly when the taste stimulus is novel (Roman, Nebieridze, Sastre, & Reilly, 2006;Roman & Reilly, 2007). These results suggest that the insular cortex has a role in gustatory neophobia.…”

Section: Introductionmentioning

confidence: 75%

NMDA receptors in the basolateral amygdala and gustatory neophobia

Figueroa-Guzmán

Reilly

2008

Brain Research

Self Cite

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The attenuation of gustatory neophobia occurs during repeated exposures to an initially novel taste solution that is increasingly perceived as safe and familiar. The present study examined whether NMDA receptors in the basolateral region of the amygdala (BLA) are involved in this important behavioral phenomenon. The results, which show that the attenuation, but not initial occurrence, of gustatory neophobia is dependent upon NMDA receptors in the BLA, are discussed with reference to a similar finding involving NMDA receptors in the insular cortex.

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“…As indicated, CTA depends on a neural circuitry involving the insular cortex, also termed gustatory or taste cortex (Bermúdez-Rattoni 2004). Lesions or functional inactivation of the insular cortex block both the acquisition and retention of CTA (Nerad et al 1996;RamirezAmaya et al 1998;Cubero et al 1999;Roman et al 2006). The insular cortex is primarily involved in the association of the gustatory and visceral stimuli (Bermúdez-Rattoni 2004).…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoids enhance taste aversion memory via actions in the insular cortex and basolateral amygdala

Miranda¹,

Quírarte²,

Rodriguez-Garcia³

et al. 2008

Learn. Mem.

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It is well established that glucocorticoid hormones strengthen the consolidation of hippocampus-dependent spatial and contextual memory. The present experiments investigated glucocorticoid effects on the long-term formation of conditioned taste aversion (CTA), an associative learning task that does not depend critically on hippocampal function. Corticosterone (1.0 or 3.0 mg/kg) administered subcutaneously to male Sprague-Dawley rats immediately after the pairing of saccharin consumption with the visceral malaise-inducing agent lithium chloride (LiCl) dose-dependently increased aversion to the saccharin taste on a 96-h retention test trial. In a second experiment, rats received corticosterone either immediately after saccharin consumption or after the LiCl injection, when both stimuli were separated by a 3-h time interval, to investigate whether corticosterone enhances memory of the gustatory or visceral stimulus presentation. Consistent with the finding that the LiCl injection, but not saccharin consumption, increases endogenous corticosterone levels, corticosterone selectively enhanced CTA memory when administered after the LiCl injection. Suppression of this training-induced release of corticosterone with the synthesis-inhibitor metyrapone (35 mg/kg) impaired CTA memory, and was dose-dependently reversed by post-training supplementation of corticosterone. Moreover, direct post-training infusions of corticosterone into the insular cortex or basolateral complex of the amygdala, two brain regions that are critically involved in the acquisition and consolidation of CTA, also enhanced CTA retention, whereas post-training infusions into the dorsal hippocampus were ineffective. These findings provide evidence that glucocorticoid effects on memory consolidation are not limited to hippocampus-dependent spatial/contextual information, but that these hormones also modulate memory consolidation of discrete-cue associative learning via actions in other brain regions.

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Effects of lesions of the bed nucleus of the stria terminalis, lateral hypothalamus, or insular cortex on conditioned taste aversion and conditioned odor aversion.

Cited by 37 publications

References 89 publications

The Way an Odor Is Experienced during Aversive Conditioning Determines the Extent of the Network Recruited during Retrieval: A Multisite Electrophysiological Study in Rats

The Way an Odor Is Experienced during Aversive Conditioning Determines the Extent of the Network Recruited during Retrieval: A Multisite Electrophysiological Study in Rats

NMDA receptors in the basolateral amygdala and gustatory neophobia

Glucocorticoids enhance taste aversion memory via actions in the insular cortex and basolateral amygdala

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