Journal
NEURON
Volume 105, Issue 6, Pages 1062-+Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2019.12.024
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Funding
- NIH [MH107435, MH114363, DA043982, NS052819]
- NARSAD Young Investigator Award
- Integrative Neuroscience Initiative on Alcoholism (INIA stress) [AA9013514]
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Functional coupling between the amygdala and the dorsomedial prefrontal cortex (dmPFC) has been implicated in the generation of negative affective states; however, the mechanisms by which stress increases amygdala-dmPFC synaptic strength and generates anxiety-like behaviors are not well understood. Here, we show that the mouse basolateral amygdala (BLA)-prelimbic prefrontal cortex (pIPFC) circuit is engaged by stress and activation of this pathway in anxiogenic. Furthermore, we demonstrate that acute stress exposure leads to a lasting increase in synaptic strength within a reciprocal BLA-pIPFC-BLA subcircuit. Importantly, we identify 2-arachidonoylglycerol (2-AG)-mediated endocannabinoid signaling as a key mechanism limiting glutamate release at BLA-pIPFC synapses and the functional collapse of multimodal 2-AG signaling as a molecular mechanism leading to persistent circuit-specific synaptic strengthening and anxiety-like behaviors after stress exposure. These data suggest that circuit-specific impairment in 2-AG signaling could facilitate functional coupling between the BLA and pIPFC and the translation of environmental stress to affective pathology.
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