Differential effects of amygdaloid lesions on conditioned taste aversion learning by rats

doi:10.1016/0031-9384(81)90322-X

Physiology & Behavior

Volume 27, Issue 3, September 1981, Pages 397-400

https://doi.org/10.1016/0031-9384(81)90322-X Get rights and content

Abstract

Rats with electrolytic lesions placed in either the basolateral or corticomedial divisions of the amygdala acquired a conditioned taste aversion to sucrose. Comparisons with a surgical control group indicated that damage to the corticomedial amygdala did not alter the animals' performance, while damage in the basolateral nuclei resulted in a small but significant attenuation of the aversion. Furthermore, these amygdaloid lesions did not alter the acceptability of two quinine hydrochloride solutions (0.01% and 0.001%). The daily drinking behavior of the rats with basolateral amygdaloid lesions appeared consistent with the hypothesis that this lesion affected the animals' appreciation of the novelty of the sucrose solution, and hence attenuated the subsequent aversion.

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Expression of c-Fos following voluntary ingestion of a novel or familiar taste in rats
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Taste neophobia, the rejection of novel tastes or foods, involves an interplay of various brain regions encompassing areas within the central gustatory system, as well as nuclei serving other functions. Previous findings, utilising c-Fos imaging, identified several brain regions which displayed higher activity after ingestion of a novel taste as compared to a familiar taste. The present study extends this analysis to include additional regions suspected of contributing to the neurocircuitry involved in evoking taste neophobia. Our data show increased c-Fos expression in the basolateral amygdala, central nucleus of the amygdala, gustatory portion of the thalamus, gustatory portion of the insular cortex and the medial and lateral regions of the parabrachial nucleus. These results confirm the contribution of areas previously identified as active during ingestion of novel tastes and expose additional areas that express elevated levels of c-Fos under these conditions, thus adding to the neural network involved in the detection and initial processing of taste novelty.
Inhibiting gustatory thalamus or medial amygdala has opposing effects on taste neophobia
2018, Neurobiology of Learning and Memory
Citation Excerpt :
Arthurs & Reilly (2013) found that the GT was also necessary for taste neophobia but that the same lesion had no influence on the rate of CTA acquisition. An examination of the literature revealed a similar pattern of results for MeA lesions: an attenuation of taste neophobia (Lin et al., 2009) that did not produce a delay in CTA acquisition (e.g., Aggleton, Petrides & Iversen, 1981; Meliza, Leung & Rogers, 1981; Rollins, Stines, McGuire & King, 2001; for a review see Reilly & Bornovalova, 2005). The fact that lesions of different structures can cause a similar attenuation of taste neophobia while having different influences on CTA acquisition suggests that taste neophobia has multiple behavioral components that are governed by different neural circuits.
Taste neophobia is a feeding system defense mechanism that limits consumption of an unknown, and therefore potentially dangerous, edible until the post-ingestive consequences are experienced. We found that transient pharmacological inhibition (induced with the GABA agonists baclofen and muscimol) of the gustatory thalamus (GT; Experiment 1), but not medial amygdala (MeA; Experiment 2), during exposure to a novel saccharin solution attenuated taste neophobia. In Experiment 3 we found that inhibition of MeA neurons (induced with the chemogenetic receptor hM4DGi) enhanced the expression of taste neophobia whereas excitation of MeA neurons (with hM3DGq) had no influence of taste neophobia. Overall, these results refine the temporal involvement of the GT in the occurrence of taste neophobia and support the hypothesis that neuronal excitation in the GT is necessary for taste neophobia. Conversely, we show that chemogenetically, but not pharmacologically, inhibiting MeA neurons is sufficient to exaggerate the expression of taste neophobia.
Taste neophobia: Neural substrates and palatability
2018, Food Neophobia: Behavioral and Biological Influences
Animals, including humans, are reluctant to eat a new food because they have no information about the content—whether it is safe to eat or poisonous. In fact, on first encounter with a novel edible, most animals will eat only a small amount of the new food and in the ensuing seconds to hours wait to discover the postingestive consequences. If the edible has no aversive systemic effects, then more of the food will be consumed on subsequent encounters until the food is recognized as safe. Conversely, if aversive postingestive effects are experienced, the animal learns to refrain from eating the food on subsequent encounters. The initial reluctance to eat the new food is termed taste (or more generally food) neophobia and the acquired knowledge that the food is poisonous is called a conditioned taste aversion (CTA). My aim in this chapter is to examine the neural substrates and nature of taste neophobia, which will also include its relationship with CTA learning. In order to provide background and perspective, I will begin by noting some of the characteristics of taste neophobia and CTA. The primary focus of the chapter, however, will be the recent research from my laboratory, which supports a novel conceptual analysis that goes beyond the scope of the traditional view of these phenomena.
Amygdala: Structure and Function
2015, The Rat Nervous System: Fourth Edition
The amygdala is considered a key center in managing emotional information and its dysfunction is at the base of disorders ranging through anxiety, depression, PTSD and autism. However, the amygdala seems heterogeneous both structurally (with pallial and supallial components) and functionally. Thus, whereas cortical and thalamic multimodal sensory inputs enter the basolateral complex, the corticomedial amygdala is dominated by olfactory and vomeronasal inputs. Intrinsic amygdaloid circuitry, connects these two amygdaloid divisions and convey processed information to the main amygdala outputs. The pallial amygdala is the main source for telencephalic outputs to associative cortical areas (e.g., frontal lobe and hippocampus) and to the ventral striatum. The two subdivisions of the extended amygdala, central and medial, originate descending projections to the hypothalamus and brainstem centers for emotional responses and behavioral control. The amygdala is the key node of the neural network where sensory information acquires emotional value through Pavlovian associations and where fear memories may be extinguished. It is also a fundamental piece of the neural machinery controlling socio-sexual and defensive behaviors.
Role of the gustatory thalamus in taste learning
2013, Behavioural Brain Research
Citation Excerpt :
A similar elevated consumption of a novel taste CS was seen in the GTX rats in the present study but this deficit appeared to have no influence on the rate of taste aversion learning. Interestingly, bilateral lesions of the medial amygdala (MeA) disrupt the initial expression of taste neophobia [33] but are reported to have no influence of CTA acquisition [1,38,55,60,66]. Finally, a recent study employing asymmetric unilateral lesions of the GC, BLA or MeA revealed that the GC and BLA form a functional unit in terms of the initial expression of taste neophobia; asymmetric unilateral lesions of the MeA and GC or MeA and BLA had no influence on taste neophobia [28].
The present study re-examined the involvement of the gustatory thalamus (GT) in the acquisition of drug- and toxin-induced conditioned taste aversions (CTAs) using a standardized procedure involving 15-min taste trials in rats injected with morphine (Experiment 1), lithium chloride (Experiment 2) or amphetamine (Experiment 3). Contrary to previous results, GT lesions did not eliminate drug-induced CTAs. Rather, GT-lesioned rats acquired aversions of comparable magnitude to non-lesioned subjects but from an elevated intake on the first conditioning trial. A similar pattern of lesion effects was found in the acquisition of an illness-induced CTA. Thus, we conclude that GT lesions do not differentially influence CTAs conditioned with drugs or toxins. The lesion-induced elevated intake of a novel tastant confirms an unappreciated role for the GT in taste neophobia.
Amygdala-gustatory insular cortex connections and taste neophobia
2012, Behavioural Brain Research
To examine whether communication between the amygdala and gustatory insular cortex (GC) is required for normal performance of taste neophobia, three experiments were conducted. In Experiment 1, rats with asymmetric unilateral lesions of the basolateral amygdala (BLA) and the GC displayed elevated intake of a novel saccharin solution relative to control subjects. However, an attenuation of neophobia was not found following asymmetric unilateral lesions of the GC and medial amygdala (MeA; Experiment 2) or of the MeA and BLA (Experiment 3). This pattern of results indicates that the BLA and GC functionally interact during expression of taste neophobia and that the MeA functionally interacts with neither the BLA nor the GC. Research is needed to further characterize the nature of the involvement of the MeA in taste neophobia and to determine the function of the BLA–GC interaction during exposure to a new taste.

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¹: Send reprint requests to current address: National Institute of Mental Health, Building 9, Room 1N107, 9000 Rockville Pike, Bethesda, MD 20205.

²: Currently at Department of Psychology, McGill University, 1205 Dr. Penfield Avenue, Montreal, Quebec, H3A 1B1 and Montreal Neurological Institute, 3801 University Street, Montreal, Quebec, H3A 2B4, Canada.

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Differential effects of amygdaloid lesions on conditioned taste aversion learning by rats

Abstract

Physiol. Behav.

Behav. Biol.

Physiol. Behav.

Behav. Biol.

Physiol. Behav.

Studies of the vertebrate telencephalon. II. The nuclear pattern of the anterior olfactory nucleus, tuberculum olfactorium and the amygdaloid complex in adult man

J. comp. Neurol.

Further contributions to the study of the evolution of the forebrain

J. comp. Neurol.