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首页> 外文期刊>Experimental Neurology >Does excitotoxic cell death of motor neurons in ALS arise from glutamate transporter and glutamate receptor abnormalities?
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Does excitotoxic cell death of motor neurons in ALS arise from glutamate transporter and glutamate receptor abnormalities?

机译:ALS中运动神经元的兴奋性毒性细胞死亡是否由谷氨酸转运蛋白和谷氨酸受体异常引起?

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摘要

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative condition resulting from progressive and selective loss of motor neurons, particularly those in the spinal cord. Despite much research, there is no single unifying consensus on the key events which underlie motor neuron cell death, and numerous mechanisms have been implicated that include enhanced oxidative stress and free radical production, abnormalities in axonal transport, protein aggregation, mitochondrial dysfunction and glutamate-mediated excitotoxicity. Excitotoxicity caused by glutamate, an endogenous neurotransmitter, is a long-standing concept and may be one of the major underlying causes of motor neuron loss in ALS. Briefly stated, glutamate excitotoxicity is a loss of control of normal glutamate transmission resulting in a calcium-mediated cell death through over activation of calcium-permeable glutamate receptors (Choi, 1988).
机译:肌萎缩性侧索硬化症(ALS)是一种致命的神经退行性疾病,是由运动神经元(尤其是脊髓中的神经元)进行性和选择性丧失所致。尽管进行了大量研究,但对于运动神经元细胞死亡的关键事件尚无统一的共识,并且涉及许多机制,包括增强的氧化应激和自由基产生,轴突运输异常,蛋白质聚集,线粒体功能障碍和谷氨酸-介导的兴奋性毒性。谷氨酸(一种内源性神经递质)引起的兴奋性毒性是一个长期存在的概念,并且可能是ALS中运动神经元丢失的主要潜在原因之一。简而言之,谷氨酸兴奋性毒性是对正常谷氨酸传递的控制的丧失,其通过钙可渗透性谷氨酸受体的过度活化而导致钙介导的细胞死亡(Choi,1988)。

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