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Pharmacological activation of the amygdala, but not single prolonged footshock-induced acute stress, interferes with cue-induced motivation toward food rewards in rats

In the face of threats, animals adapt their behaviors to cope with the situation. Under such circumstances, irrelevant behaviors are usually suppressed. In this study, we examined whether food-seeking motivation would decrease under activation of the amygdala, an important nucleus in the regulation...

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Autores principales: Lai, Chien-Wen, Chang, Chun-hui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10538645/
https://www.ncbi.nlm.nih.gov/pubmed/37781505
http://dx.doi.org/10.3389/fnbeh.2023.1252868
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author Lai, Chien-Wen
Chang, Chun-hui
author_facet Lai, Chien-Wen
Chang, Chun-hui
author_sort Lai, Chien-Wen
collection PubMed
description In the face of threats, animals adapt their behaviors to cope with the situation. Under such circumstances, irrelevant behaviors are usually suppressed. In this study, we examined whether food-seeking motivation would decrease under activation of the amygdala, an important nucleus in the regulation of stress response in the central nervous system, or after a physical acute stress session. In Experiment 1, we pharmacologically activated the basolateral nucleus (BLA) or the central nucleus of the amygdala (CeA) before a cue-induced reinstatement test in rats. Our results showed that activation of the BLA or the CeA abolished cue-induced motivation toward food rewards, while locomotor activity and free food intake were not affected. In Experiments 2 and 3, we further assessed anxiety and despair levels, as well as cue-induced reinstatement, after a single prolonged footshock-induced acute stress in rats. Behaviorally, acute stress did not affect anxiety level, despair level, or cue-induced motivation toward food rewards. Physiologically, there was no difference in cellular activities of the amygdala immediately after acute stress. To conclude, our results suggested that pharmacological activation of the amygdala decreased cue-induced motivation toward food reward. However, physiological acute stress did not immediately interfere with the negative emotions, motivation, or amygdala activities of the animals.
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spelling pubmed-105386452023-09-29 Pharmacological activation of the amygdala, but not single prolonged footshock-induced acute stress, interferes with cue-induced motivation toward food rewards in rats Lai, Chien-Wen Chang, Chun-hui Front Behav Neurosci Behavioral Neuroscience In the face of threats, animals adapt their behaviors to cope with the situation. Under such circumstances, irrelevant behaviors are usually suppressed. In this study, we examined whether food-seeking motivation would decrease under activation of the amygdala, an important nucleus in the regulation of stress response in the central nervous system, or after a physical acute stress session. In Experiment 1, we pharmacologically activated the basolateral nucleus (BLA) or the central nucleus of the amygdala (CeA) before a cue-induced reinstatement test in rats. Our results showed that activation of the BLA or the CeA abolished cue-induced motivation toward food rewards, while locomotor activity and free food intake were not affected. In Experiments 2 and 3, we further assessed anxiety and despair levels, as well as cue-induced reinstatement, after a single prolonged footshock-induced acute stress in rats. Behaviorally, acute stress did not affect anxiety level, despair level, or cue-induced motivation toward food rewards. Physiologically, there was no difference in cellular activities of the amygdala immediately after acute stress. To conclude, our results suggested that pharmacological activation of the amygdala decreased cue-induced motivation toward food reward. However, physiological acute stress did not immediately interfere with the negative emotions, motivation, or amygdala activities of the animals. Frontiers Media S.A. 2023-09-14 /pmc/articles/PMC10538645/ /pubmed/37781505 http://dx.doi.org/10.3389/fnbeh.2023.1252868 Text en Copyright © 2023 Lai and Chang. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Behavioral Neuroscience
Lai, Chien-Wen
Chang, Chun-hui
Pharmacological activation of the amygdala, but not single prolonged footshock-induced acute stress, interferes with cue-induced motivation toward food rewards in rats
title Pharmacological activation of the amygdala, but not single prolonged footshock-induced acute stress, interferes with cue-induced motivation toward food rewards in rats
title_full Pharmacological activation of the amygdala, but not single prolonged footshock-induced acute stress, interferes with cue-induced motivation toward food rewards in rats
title_fullStr Pharmacological activation of the amygdala, but not single prolonged footshock-induced acute stress, interferes with cue-induced motivation toward food rewards in rats
title_full_unstemmed Pharmacological activation of the amygdala, but not single prolonged footshock-induced acute stress, interferes with cue-induced motivation toward food rewards in rats
title_short Pharmacological activation of the amygdala, but not single prolonged footshock-induced acute stress, interferes with cue-induced motivation toward food rewards in rats
title_sort pharmacological activation of the amygdala, but not single prolonged footshock-induced acute stress, interferes with cue-induced motivation toward food rewards in rats
topic Behavioral Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10538645/
https://www.ncbi.nlm.nih.gov/pubmed/37781505
http://dx.doi.org/10.3389/fnbeh.2023.1252868
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