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Interhemispheric connectivity potentiates the basolateral amygdalae and regulates social interaction and memory

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Huang, T-N, Hsu, T-T, Lin, M-H, Chuang, H-C, Hu, H-T, Sun, C-P, Tao, M-H, Lin, JY ORCID: 0000-0002-1723-4597, Chuang, H-C, Sun, C-P, Tao, M-H, Lin, JY ORCID: 0000-0002-1723-4597 and Hsueh, Y-P 2019 , 'Interhemispheric connectivity potentiates the basolateral amygdalae and regulates social interaction and memory' , Cell reports, vol. 29, no. 1 , pp. 34-48 , doi: 10.1016/j.celrep.2019.08.082.

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Abstract

Impaired interhemispheric connectivity is commonly found in various psychiatric disorders, although how interhemispheric connectivity regulates brain function remains elusive. Here, we use the mouse amygdala, a brain region that is critical for social interaction and fear memory, as a model to demonstrate that contralateral connectivity intensifies the synaptic response of basolateral amygdalae (BLA) and regulates amygdala-dependent behaviors. Retrograde tracing and c-FOS expression indicate that contralateral afferents widely innervate BLA non-randomly and that some BLA neurons innervate both contralateral BLA and the ipsilateral central amygdala (CeA). Our optogenetic and electrophysiological studies further suggest that contralateral BLA input results in the synaptic facilitation of BLA neurons, thereby intensifying the responses to cortical and thalamic stimulations. Finally, pharmacological inhibition and chemogenetic disconnection demonstrate that BLA contralateral facilitation is required for social interaction and memory. Our study suggests that interhemispheric connectivity potentiates the synaptic dynamics of BLA neurons and is critical for the full activation and functionality of amygdalae.

Item Type: Article
Authors/Creators:Huang, T-N and Hsu, T-T and Lin, M-H and Chuang, H-C and Hu, H-T and Sun, C-P and Tao, M-H and Lin, JY and Chuang, H-C and Sun, C-P and Tao, M-H and Lin, JY and Hsueh, Y-P
Keywords: Neurocircuit, optogenetics, chemogenetics, electrophysiology
Journal or Publication Title: Cell reports
Publisher: Cell Press
ISSN: 2211-1247
DOI / ID Number: 10.1016/j.celrep.2019.08.082
Copyright Information:

Copyright 2019 the authors. Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) https://creativecommons.org/licenses/by-nc-nd/4.0/

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