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The present study established a rat cortical neuronal model of in vitro mechanical injury.At 30 mi-nutes after injury,the survival rate of the injured cortical neurons was decreased compared with normal neurons,and was gradually decreased with aggravated degree of injury.Reverse transcription-polymerase chain reaction results showed that at 1 hour after injury,there was increased expression of metabotropic glutamate receptor 1a in cortical neurons.Immunohistochemical staining results showed that at 30 minutes after injury,the number of metabotropic glutamate receptor 1a-positive cells increased compared with normal neurons.At 12 hours after injury,lactate dehydrogenase activity in the (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA)-treated injury neurons was significantly decreased than that in the pure injury group.At 1 hour after injury,intracellular free Ca2+ concentration was markedly decreased in the AIDA-treated injury neurons than that in the pure injury neurons.These findings suggest that after mechanical injury to cortical neurons,metabotropic glutamate receptor 1a expression increased.The resulting increase in intracellular free Ca2+ concentration was blocked by AIDA,indicating that AIDA exhibits neuroprotective effects after mechanical injury.
The present study established a rat cortical neuronal model of in vitro mechanical injury. At 30 mi-nutes after injury, the survival rate of the injured cortical neurons was decreased compared with normal neurons, and was gradually decreased with aggravated degree of injury. Reverse transcription -polymerase chain reaction results showed that at 1 hour after injury, there was increased expression of metabotropic glutamate receptor 1a in cortical neurons. Immunohistochemical staining results showed that at 30 minutes after injury, the number of metabotropic glutamate receptor 1a-positive cells increased compared with normal neurons. At 12 hours after injury, lactate dehydrogenase activity in the (RS) -1-aminoindan-1,5-dicarboxylic acid (AIDA) -treated injury neurons was significantly decreased than that in the pure wound group. At 1 hour after injury, intracellular free Ca2 + concentration was markedly decreased in the AIDA-treated injury neurons than that in the pure injury neurons. These findings su ggest that after mechanical injury to cortical neurons, metabotropic glutamate receptor 1a expression increased. The resulting in intracellular free Ca2 concentration was blocked by AIDA, indicating that AIDA exhibits neuroprotective effects after mechanical injury.