The roles of mGluR 4 and its agonist L-AP 4 following diffuse brain injury
Abstract:Objective The focus of this study is to examine the roles of mGluR 4 after diffuse brain injury(DBI) and its specific agonist L-AP 4.Methods 161 male SD rats were randomized into two groups. Group A included normal control, sham-operated control and DBI group. DBI was produced by Marmarou's diffuse brain injury model. The mRNA expression of mGluR 4 was detected by hybridization in situ. Group B included DBI alone, DBI treated with normal saline and DBI treated with L-AP 4. All DBI rats were first trained in a series of performance tests before they were subjected to DBI. At 1 and 12 h, animals were injected intracerebroventricularly with L-AP 4(100 mM, 10 μl) or normal saline respectively. The rats were tested for motor and cognitive performance respectively at 1, 3, 7, 14 d post injury and then were killed for detecting the damaged neurons.Results There was no significant difference between normal control group and sham-operated group in the expression of mGluR 4(P>0.05). The animals exposed to DBI showed a significantly increased expression of mRNA of mGluR 4 compared with the sham-operated animals 1 h after injury(P<0.05). At 6 h, the evolution of neuronal expression of mGluR 4 in the trauma alone group was relatively static. Compared with saline-treated control animals, the rats treated with L-AP 4 showed decreased number of damaged neurons and a better motor and cognitive performance.Conclusion It is indicated that the increased expression of mGluR 4 is an important process in the pathophysiological changes of DBI and its specific agonist L-AP 4 can provide a remarkable neuroprotection.
Keywords:Diffuse brain injuryMetabotropic glutamate receptors
Publication Date:2003-01-01
Online Publishing Date:2025-08-15(First online date of this platform, not the publication date of the document)
Pages:7( 196-202 )
Chinese Journal of Neurosurgical Disease Research

Chinese Journal of Neurosurgical Disease Research

ISTIC
ISSN:1671-2897
Year, Vol.(Issue):2003,2(3)