AI Article Synopsis
- Chronic predator stress (CPS) affects anhedonia in animals, and this study identifies specific neural circuits that are involved in this effect.
- Corticotropin-releasing hormone (CRH) neurons in the medial subthalamic nucleus (mSTN) are found to enhance struggle behaviors and contribute to anhedonia largely through their connections to the external globus pallidus (GPe).
- CPS alters the responsiveness of mSTN-CRH neurons to different stimuli, and enhanced inputs from the bed nucleus of the stria terminalis (BNST) are implicated in mediating behaviors associated with despair and anhedonia, shedding light on neurocircuitry linked to defense mechanisms
Article Abstract
Chronic predator stress (CPS) is an important and ecologically relevant tool for inducing anhedonia in animals, but the neural circuits underlying the associated neurobiological changes remain to be identified. Using cell-type-specific manipulations, we found that corticotropin-releasing hormone (CRH) neurons in the medial subthalamic nucleus (mSTN) enhance struggle behaviors in inescapable situations and lead to anhedonia, predominately through projections to the external globus pallidus (GPe). Recordings of in vivo neuronal activity revealed that CPS distorted mSTN-CRH neuronal responsivity to negative and positive stimuli, which may underlie CPS-induced behavioral despair and anhedonia. Furthermore, we discovered presynaptic inputs from the bed nucleus of the stria terminalis (BNST) to mSTN-CRH neurons projecting to the GPe that were enhanced following CPS, and these inputs may mediate such behaviors. This study identifies a neurocircuitry that co-regulates escape response and anhedonia in response to predator stress. This new understanding of the neural basis of defensive behavior in response to predator stress will likely benefit our understanding of neuropsychiatric diseases.
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| http://dx.doi.org/10.1016/j.nbd.2024.106649 | DOI Listing |
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