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Amygdala is widely known as a critical neural hub for modulating negative emotions such as fear and anxiety. Recent studies have shown that the basolateral amygdala (BLA) has reciprocal innervation, which plays an important role in regulating social interaction and associative memory. However, the connectivity pattern and functional role of the contralateral projecting BLA neurons in stress-related anxiety are not fully understood. Here, using the virus tracing strategy, we first characterized the connectivity pattern of the contralateral projecting neurons in BLA. Then, we examined the effect of stress on the functional changes of those specific neuronal populations using a mouse model of inescapable footshock stress. The results showed that the fibers of the contralateral projecting BLA neurons labeled by enhanced green fluorescent protein (EGFP) have no collateral projections to the ipsilateral or contralateral hippocampus. Interestingly, they have some collateral projections to the ipsilateral medial prefrontal cortex. Behavioral results showed that footshock stress increases the anxiety-like behavior in mice; however, the excitatory synaptic transmission and intrinsic excitability of the contralateral projecting BLA neurons measured by whole-cell patch clamp recording did not change after stress exposure. In conclusion, our results indicate that contralateral projecting BLA neurons may not contribute to footshock stress-related anxiety-like behavior.


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Connectivity and functional characterization of the mouse contralateral projecting neurons in basolateral amygdala

Show Author's information Jia-Xin Zou1,2Guan-Qun Shang3Wei-Zhu Liu1,2Ye He4( )Wen-Hua Zhang1,2( )
Department of Biological Science, School of Life Science, Nanchang University, Nanchang 330031, China
Laboratory of Fear and Anxiety Disorders, Institutes of Life Science, Nanchang University, Nanchang 330031, China
Queen Mary School, Nanchang University, Nanchang 330001, China
School of Basic Medical Sciences, Nanchang University, Nanchang 330031, China

Abstract

Amygdala is widely known as a critical neural hub for modulating negative emotions such as fear and anxiety. Recent studies have shown that the basolateral amygdala (BLA) has reciprocal innervation, which plays an important role in regulating social interaction and associative memory. However, the connectivity pattern and functional role of the contralateral projecting BLA neurons in stress-related anxiety are not fully understood. Here, using the virus tracing strategy, we first characterized the connectivity pattern of the contralateral projecting neurons in BLA. Then, we examined the effect of stress on the functional changes of those specific neuronal populations using a mouse model of inescapable footshock stress. The results showed that the fibers of the contralateral projecting BLA neurons labeled by enhanced green fluorescent protein (EGFP) have no collateral projections to the ipsilateral or contralateral hippocampus. Interestingly, they have some collateral projections to the ipsilateral medial prefrontal cortex. Behavioral results showed that footshock stress increases the anxiety-like behavior in mice; however, the excitatory synaptic transmission and intrinsic excitability of the contralateral projecting BLA neurons measured by whole-cell patch clamp recording did not change after stress exposure. In conclusion, our results indicate that contralateral projecting BLA neurons may not contribute to footshock stress-related anxiety-like behavior.

Keywords: anxiety, amygdala, stress, contralateral connectivity, circuit

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Publication history

Received: 15 July 2022
Revised: 11 August 2022
Accepted: 24 August 2022
Published: 09 September 2022
Issue date: September 2022

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© The Author(s) 2022

Acknowledgements

This work was supported by grants from the National Natural Science Foundation of China (No. 81930032 to P.B., No. 31970953 to Z.W., and No. 82125010 to P.B.), National Key R & D Program of China (No. 2021ZD0202704 to P.B.), and Natural Science Foundation of Jiangxi Province (No. 20212ACB206038 to Z.W.).

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