The Role of Posttraumatic Hypothermia in Preventing Dendrite Degeneration and Spine Loss after Severe Traumatic Brain Injury.
Posttraumatic hypothermia prevents cell death and promotes functional outcomes after traumatic brain injury (TBI). However, little is known regarding the effect of hypothermia on dendrite degeneration and spine loss after severe TBI. In the present study, we used thy1-GFP transgenic mice to investigate the effect of hypothermia on the dendrites and spines in layer V/VI of the ipsilateral cortex after severe TBI. We found that hypothermia (33 °C) dramatically prevented dendrite degeneration and spine loss 1 and 7 days after CCI. The Morris water maze test revealed that hypothermia preserved the learning and memory functions of mice after CCI. Hypothermia significantly increased the expression of the synaptic proteins GluR1 and PSD-95 at 1 and 7 days after CCI in the ipsilateral cortex and hippocampus compared with that of the normothermia TBI group. Hypothermia also increased cortical and hippocampal BDNF levels. These results suggest that posttraumatic hypothermia is an effective method to prevent dendrite degeneration and spine loss and preserve learning and memory function after severe TBI. Increasing cortical and hippocampal BDNF levels might be the mechanism through which hypothermia prevents dendrite degeneration and spine loss and preserves learning and memory function.
Department of Neurosurgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, People's Republic of China.|Shanghai Institute of Head Trauma, Shanghai 200127, People's Republic of China.
Chuan-Fang
CF
Wang
Department of Neurosurgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, People's Republic of China.|Shanghai Institute of Head Trauma, Shanghai 200127, People's Republic of China.
Cheng-Cheng
CC
Zhao
Department of Pharmacology, Institute of Medical Science, Shanghai Jiaotong University School of Medicine, Shanghai 200127, People's Republic of China.
Gan
G
Jiang
Department of Pharmacology, Institute of Medical Science, Shanghai Jiaotong University School of Medicine, Shanghai 200127, People's Republic of China.
Xiao
X
Gu
Department of Neurosurgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, People's Republic of China.|Shanghai Institute of Head Trauma, Shanghai 200127, People's Republic of China.
Jun-Feng
JF
Feng
Department of Neurosurgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, People's Republic of China.|Shanghai Institute of Head Trauma, Shanghai 200127, People's Republic of China.
Ji-Yao
JY
Jiang
D000818:Animals; D000070642:Brain Injuries, Traumatic / Q000473:pathology* / Q000503:physiopathology*; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology*; D049229:Dendritic Spines / Q000473:pathology*; D000076122:Disks Large Homolog 4 Protein / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism; D007036:Hypothermia, Induced; D008297:Male; D018782:Maze Learning; D051379:Mice; D008822:Mice, Transgenic; D018091:Receptors, AMPA / Q000378:metabolism; D013569:Synapses / Q000378:metabolism
D019208:Brain-Derived Neurotrophic Factor; D000076122:Disks Large Homolog 4 Protein; D018091:Receptors, AMPA; C501447:Dlg4 protein, mouse