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The immature brain needs GABA to be excited and hyper-excited.

机译:未成熟的大脑需要GABA兴奋和过度兴奋。

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The perspective article 'Immature brains don't need GABA to get "hyper"-excited', Goaillard (2010) highlights the paper of Shao & Dudek (2009) who suggested that seizures generated in 'immature' CA3 slices by GABA_A receptor blockers do not depend on the excitatory action of GABA, but on other mechanisms including intrinsic parameters, release properties, recurrent synaptic connections, etc. From this work centred on epilepsies, Goaillard challenges whether GABA excites immature neurons at all, as suggested two decades ago and repeatedly confirmed. It is important to stress that Dudek and Shao conducted their study on CA3 neurons recorded from third week animals when the developmental shift of GABA has already occurred thereby mixing two different issues: the developmental sequence and the effects of seizures. Indeed, GABA can excite adult epileptic neurons because of intracellular chloride accumulation (Cohen et al. 2002). Indeed, Goaillard challenges the concept that GABA excites immature neurons (at an earlier age) relying on the study of Rheims et al. (2009) who claimed that the depolarizing action of GABA is an artifact due to energy deprivation in slices where glucose is the sole metabolic source.
机译:观点文章“未成熟的大脑不需要GABA来获得“过度”兴奋”,Goaillard(2010)强调了Shao&Dudek(2009)的论文,他提出GABA_A受体阻滞剂会在“未成熟” CA3切片中引起癫痫发作不依赖于GABA的兴奋作用,而是依赖于其他机制,包括内在参数,释放特性,复发性突触连接等。根据这项以癫痫为中心的研究,Goaillard质疑了GABA是否完全激发未成熟的神经元,正如二十年前提出的那样。确认。需要强调的是,当GABA的发育已经发生时,Dudek和Shao对第三周动物记录的CA3神经元进行了研究,从而混合了两个不同的问题:发育顺序和癫痫发作的影响。实际上,由于细胞内氯化物的积累,GABA可以激发成年的癫痫神经元(Cohen等,2002)。的确,Goaillard依靠Rheims等人的研究挑战了GABA激发未成熟神经元(在较早的年龄)的概念。 (2009年),他声称GABA的去极化作用是由于切片中能量的缺乏导致的伪影,其中葡萄糖是唯一的代谢来源。

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