Subarachnoid Hemorrhage Induces mPFC CRF Neuronal Dysfunction Leading to Anxiety and Depression in Male Mice

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.