Dysfunction of mPFC CRF neurons is a key contributor to anxiety and depression after SAH. Basolateral amygdala inputs modulate mPFC CRF neuron activity, and SYT9 downregulation represents a critical molecular mechanism underlying their impairment. These findings identify mPFC CRF neuronal dysfunction as a core pathological feature of SAH-induced affective disorders and provide mechanistic insight into potential therapeutic targets.
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Jin Yan
Fuming Liang
Na Wu
Stroke
Chongqing Medical University
Children's Hospital of Chongqing Medical University
Affiliated Hospital of Southwest Medical University
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Yan et al. (Mon,) studied this question.
www.synapsesocial.com/papers/69df2ba0e4eeef8a2a6b0a8a — DOI: https://doi.org/10.1161/strokeaha.125.054572
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