A study on the mechanism of MPP^+ neurotoxicity in culture of fatal rat doperminergic neurons

为探讨MPP^+对多巴胺能神经元（DN）的神经毒性作用机制，采用自由基、神经生长因子、我们已经证明DN可能只对加入胶质细胞促有丝分裂因子如表皮生长因子和碱性成纤维细胞后引起的酸度升高敏感DN对酸的敏感性是DN特有的，脑源性神经营养因子（BDNF）可抑制这种敏感性。VE、VC、CoQ_2和过氧化氢酶等抗氧化剂<10>可减轻MPP^+诱导的DN死亡，而谷氨酸受体不能改变MPP^+的神经毒性，但别嘌呤醇和超氧化物歧化酶均不能减轻MPP ^+诱导的DN死亡。IL-1 β在DN中起神经营养因子的作用，而IL-6在不引起神经胶质细胞增生的情况下能够保护DN免受MPP^+的神经毒性。

To study on the mechanism of MPP^+ neurotoxicity against doperminergic neurons (DN), the vulneravility of cultured cells from the ventral mesencephalon of embryonic 17 days rats under MPP^+ was evaluated with free radical, nerve growth factor, or interleukin.We have shown that DN may be exclusively sensitive to elevated acidity elicited after the addition of glial mitogenic factors such as epidermal growth factor and basic fibroblast growth factor or after the direct treatment with hydrochloric acid.The acid sensitivity was specific to DN and was inhibited by addition of brain-derived neurotrophic factor (BDNF).Such antioxidants as VE,VC,CoQ_<10> and catalase, but neither allopurinol nor superoxide dismutase, alleviated the MPP^+ induced death of DN,while glutamate receptor did not alter MPP^+ neurotoxicity.Concerning interleukin (IL), IL-1beta was showed to act as a neurotrophic factor on DN,and IL-6 was revealed to be able of protecting DN from the neurotoxicity of MPP^+ without glial proliferation.