Objective: To examine the changes in the express ion of mGluR4 after diffuse brain injury (DBI) and to determine the role of its specific agonist L-2-amino-4-phosphonobutyrate (L-AP4) in vivo. Methods: A total of 161 ...Objective: To examine the changes in the express ion of mGluR4 after diffuse brain injury (DBI) and to determine the role of its specific agonist L-2-amino-4-phosphonobutyrate (L-AP4) in vivo. Methods: A total of 161 male SD rats were randomized into the f ollowing groups. Group A included normal control,sham-operated control and DBI group. DBI was produced according to Marmarous diffuse head injury model. mRN A expression of mGluR4 was detected by hybridization in situ. Group B included D BI alone,DBI treated with normal saline and DBI treated with L-AP4. All DBI ra ts were trained in a series of performance tests,following which they were subj ected to DBI. At 1 and 12 hours,animals were injected intraventricularly with L -AP4 ( 100 mmol/L ,10 μl) or normal saline. Motor and cognitive performance s were tested at 1,3,7,14 days after injury and the damaged neurons were also detected. Results: There was no significant difference between normal con trol group and sham-operated group in the expression of mGluR4 ( P > 0.05 ) . The animals exposed to DBI showed significantly increased expression of mRNA o f mGluR4 compared with the sham-operated animals 1 h after injury ( P < 0.05 ). At 6 hours,the evolution of neuronal expression of mGluR4 in the trauma al one group was relatively static. Compared with saline-treated control animals,rats treated with L-AP4 showed an effective result of decreased number of damag ed neurons and better motor and cognitive performances.Conclusions: Increased expression of mGluR4 is important in the pathophysiological process of DBI and its specific agonist L-AP4 can provide r emarkable neuroprotection against DBI not only at the histopathological level bu t also in the motor and cognitive performance.展开更多
文摘Objective: To examine the changes in the express ion of mGluR4 after diffuse brain injury (DBI) and to determine the role of its specific agonist L-2-amino-4-phosphonobutyrate (L-AP4) in vivo. Methods: A total of 161 male SD rats were randomized into the f ollowing groups. Group A included normal control,sham-operated control and DBI group. DBI was produced according to Marmarous diffuse head injury model. mRN A expression of mGluR4 was detected by hybridization in situ. Group B included D BI alone,DBI treated with normal saline and DBI treated with L-AP4. All DBI ra ts were trained in a series of performance tests,following which they were subj ected to DBI. At 1 and 12 hours,animals were injected intraventricularly with L -AP4 ( 100 mmol/L ,10 μl) or normal saline. Motor and cognitive performance s were tested at 1,3,7,14 days after injury and the damaged neurons were also detected. Results: There was no significant difference between normal con trol group and sham-operated group in the expression of mGluR4 ( P > 0.05 ) . The animals exposed to DBI showed significantly increased expression of mRNA o f mGluR4 compared with the sham-operated animals 1 h after injury ( P < 0.05 ). At 6 hours,the evolution of neuronal expression of mGluR4 in the trauma al one group was relatively static. Compared with saline-treated control animals,rats treated with L-AP4 showed an effective result of decreased number of damag ed neurons and better motor and cognitive performances.Conclusions: Increased expression of mGluR4 is important in the pathophysiological process of DBI and its specific agonist L-AP4 can provide r emarkable neuroprotection against DBI not only at the histopathological level bu t also in the motor and cognitive performance.
