51. Effects of mild induced hypothermia on hippocampal connexin 43 and glutamate transporter 1 expression following traumatic brain injury in rats.
- Author
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Li YH, Zhang CL, Zhang XY, Zhou HX, and Meng LL
- Subjects
- Animals, Brain Edema etiology, Brain Edema pathology, Brain Edema therapy, Brain Injuries pathology, Brain Injuries therapy, Connexin 43 genetics, Disease Models, Animal, Excitatory Amino Acid Transporter 2 genetics, Gene Expression, Hippocampus pathology, Immunohistochemistry, Male, Maze Learning, Memory, Rats, Up-Regulation, Brain Injuries metabolism, Connexin 43 metabolism, Excitatory Amino Acid Transporter 2 metabolism, Hippocampus metabolism, Hypothermia, Induced
- Abstract
Traumatic brain injury (TBI) is a common cause of worldwide disability and mortality. Currently, the incidence and prevalence of TBI is markedly increasing and an effective therapy is lacking. Therapeutic hypothermia (32‑35˚C) has been reported to reduce intracranial pressure and induce putative neuroprotective effects. However, the underlying molecular mechanisms remain to be elucidated. The aim of the present study was to investigate the effects of mild induced hypothermia (MIH) on the expression of connexin 43 (Cx43) and glutamate transporter 1 (GLT‑1) in the hippocampus following TBI in rats. A rat model of TBI was created using a modified weight‑drop device, followed by 4 h of hypothermia (33˚C) or normothermia (37˚C). A wet‑dry weight method was used to assess brain edema and spatial learning ability was evaluated using a Morris water maze. The levels of Cx43 and GLT‑1 were detected by immunohistochemical and western blot analysis, respectively. The results demonstrated that MIH treatment improved TBI‑induced brain edema and neurological function deficits. In addition, therapeutic MIH significantly downregulated Cx43 expression and upregulated the levels of GLT‑1 in the hippocampus post‑TBI. These findings suggested that treatment with MIH may provide a novel neuroprotective therapeutic strategy for TBI through reversing the increase in Cx43 protein and the decrease in GLT‑1.
- Published
- 2015
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