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Updated: Jul 4, 2026
Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
Oligodendrocyte prosaposin restores subarachnoid haemorrhage-induced consciousness impairment
Haiying Li1,2, Xiang Li3,4, Zhongmou Xu3,4
1Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, Jiangsu, China. lhy1015@suda.edu.cn.
Subarachnoid haemorrhage (SAH) is a life-threatening cerebrovascular event frequently accompanied by consciousness disturbances, yet the underlying mechanisms remain poorly defined. Here, we identify oligodendrocytic prosaposin (PSAP) as a critical regulator of thalamocortical connectivity and consciousness following SAH. Using multimodal approaches, including electroencephalogram and electromyogram recordings, optogenetics, single-nucleus RNA sequencing, patch-clamp recording, and magnetic resonance imaging, we demonstrate that SAH disrupts the central lateral thalamus to medial prefrontal cortex pathway via Psap downregulation in oligodendrocytes, leading to impaired PSAP-GPR37 interactions, myelin damage and functional connectivity loss. Psap overexpression or recombinant human PSAP administration restored PSAP-GPR37 interactions, preserved myelin structure and rescued central lateral thalamus to medial prefrontal cortex connectivity after SAH, resulting in improved consciousness and spatial memory. Our findings highlight oligodendrocyte dysfunction as a key mechanism underlying SAH-induced disorders of consciousness and identify PSAP as a potential therapeutic target.
Subarachnoid haemorrhage (SAH) is a life-threatening cerebrovascular event frequently accompanied by consciousness disturbances, yet the underlying mechanisms remain poorly defined. Here, we identify oligodendrocytic prosaposin (PSAP) as a critical regulator of thalamocortical connectivity and consciousness following SAH. Using multimodal approaches, including electroencephalogram and electromyogram recordings, optogenetics, single-nucleus RNA sequencing, patch-clamp recording, and magnetic resonance imaging, we demonstrate that SAH disrupts the central lateral thalamus to medial prefrontal cortex pathway via Psap downregulation in oligodendrocytes, leading to impaired PSAP-GPR37 interactions, myelin damage and functional connectivity loss. Psap overexpression or recombinant human PSAP administration restored PSAP-GPR37 interactions, preserved myelin structure and rescued central lateral thalamus to medial prefrontal cortex connectivity after SAH, resulting in improved consciousness and spatial memory. Our findings highlight oligodendrocyte dysfunction as a key mechanism underlying SAH-induced disorders of consciousness and identify PSAP as a potential therapeutic target.
