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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Chloride influx aggravates Ca2+-dependent AMPA receptor-mediated motoneuron death.
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Chloride influx aggravates Ca2+-dependent AMPA receptor-mediated motoneuron death.

机译：氯化物的涌入加剧了依赖Ca2 +的AMPA受体介导的运动神经元死亡。

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摘要

AMPA receptor-mediated excitotoxicity has been implicated in the pathogenesis of stroke, neurotrauma, epilepsy, and many neurodegenerative diseases such as motoneuron disease. We studied the role of Cl- in AMPA receptor-mediated Ca2+-dependent excitotoxicity in cultured rat spinal motoneurons. Using the gramicidin perforated patch-clamp technique, the intracellular Cl- concentration could be calculated from the reversal potential of the GABA-induced current. The membrane depolarization caused by AMPA receptor stimulation resulted in Cl- influx through 5-nitro-2(3-phenylpropyl-amino) benzoic acid- and niflumic acid-sensitive Cl- channels. Cl- influx during AMPA receptor stimulation aggravated excitotoxic motoneuron death by two mechanisms: an increase of AMPA receptor conductance and an elevation of the Ca2+ driving force through a partial repolarization. The Cl- influx during AMPA receptor stimulation was enhanced by coadministration of GABA. This resulted in an increased Ca2+ influx and an enhanced cell death, suggesting that concomitant GABAergic stimulation may aggravate excitotoxic motoneuron death.
机译：AMPA受体介导的兴奋性毒性与中风，神经创伤，癫痫和许多神经退行性疾病（例如运动神经元疾病）的发病机理有关。我们研究了在培养的大鼠脊髓运动神经元中，AMPA受体介导的Ca2 +依赖性兴奋性毒性中Cl-的作用。使用短杆菌肽穿孔膜片钳技术，可以从GABA诱导的电流的反向电位计算细胞内Cl浓度。由AMPA受体刺激引起的膜去极化导致Cl-通过5-硝基-2（3-苯丙基-氨基）苯甲酸和尼氟酸敏感的Cl-通道流入。 AMPA受体刺激过程中的Cl-内流通过两种机制加重了兴奋毒性运动神经元的死亡：AMPA受体电导的增加和通过部分复极化导致Ca2 +驱动力的升高。共同施用GABA可增强AMPA受体刺激期间的Cl内流。这导致增加的Ca2 +内流和增加的细胞死亡，表明伴随的GABA能刺激可能加剧兴奋性中毒性运动神经元的死亡。

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