Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2003
Changes of metabotropic glutamate receptor subtype 1a in diffuse brain injury with secondary brain insults and the effects of 2-methyl-4-carboxyphenylglycine.
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Fei Zhou, Zhang Xiang, Liu En-Yu
Аннотация
OBJECTIVE: To observe the changes of metabotropic glutamate receptor 1a in rat brain in a rodent model of diffuse head injury with secondary insults and the effects of 2-methyl-4-carboxyphenylglycine (MCPG).
METHODS: Based on Marmarous rodent model of diffuse brain injury (DBI), hypotension was made by blood withdrawal as secondary brain insults (SBI). 105 male SD rats were randomized into A and B groups. The changes of mGluR(1a) in cerebral cortex were studied by immunohistochemistry and the effect of MCPG by HE. Each group was divided into different subgroups at different time after injury.
RESULTS: Compared with that of sham group, the number of mGluR(1a) positive neuron increased by 12.9+/-3.2 (P<0.05) 1 day after injury in the injured cerebral cortex in DBI group. However, in DBI and SBI group there was a more significant increase in the number of mGluR(1a) positive neuron at 4 hours after injury (15.6+/-3.0, P<0.05) and then the number of mGluR(1a) positive neuron gradually decreased. Administration of MCPG reduced total cortical necrotic neurons counts on the 7th day after injury (5.21+/-2.52, P<0.05).
CONCLUSIONS: Brain injury can increase the gene expression of mGluR(1a) and the role of mGluR(1a) may be a key factor in the aggravation of head injury with SBI, and that MCPG may have therapeutic potential in head injury.
METHODS: Based on Marmarous rodent model of diffuse brain injury (DBI), hypotension was made by blood withdrawal as secondary brain insults (SBI). 105 male SD rats were randomized into A and B groups. The changes of mGluR(1a) in cerebral cortex were studied by immunohistochemistry and the effect of MCPG by HE. Each group was divided into different subgroups at different time after injury.
RESULTS: Compared with that of sham group, the number of mGluR(1a) positive neuron increased by 12.9+/-3.2 (P<0.05) 1 day after injury in the injured cerebral cortex in DBI group. However, in DBI and SBI group there was a more significant increase in the number of mGluR(1a) positive neuron at 4 hours after injury (15.6+/-3.0, P<0.05) and then the number of mGluR(1a) positive neuron gradually decreased. Administration of MCPG reduced total cortical necrotic neurons counts on the 7th day after injury (5.21+/-2.52, P<0.05).
CONCLUSIONS: Brain injury can increase the gene expression of mGluR(1a) and the role of mGluR(1a) may be a key factor in the aggravation of head injury with SBI, and that MCPG may have therapeutic potential in head injury.