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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Direct and indirect enhancement of GABAergic neurotransmission by ammonia: implications for the pathogenesis of hyperammonemic syndromes.
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Direct and indirect enhancement of GABAergic neurotransmission by ammonia: implications for the pathogenesis of hyperammonemic syndromes.

机译：氨直接和间接增强GABA能神经传递：对高氨血症综合征发病机制的影响。

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摘要

Experimental evidence indicates that ammonia causes neuroexcitation and seizures. This contrasts with the lethargy, confusion and other manifestations of global CNS depression commonly considered to be major components of hyperammonemic encephalopathies. Substantial data now indicates that ammonia can modulate GABAergic neurotransmission through direct and indirect mechanisms. This modulation consists of an enhancement of GABAergic neurotransmission at concentrations commonly encountered in hyperammonemic states and precedes the suppression of inhibitory neuronal function observed at higher (>1mM) ammonia concentrations. Not only is this increase in GABAergic neurotransmission consistent with the clinical picture of lethargy, ataxia and cognitive deficits associated with liver failure and congenital hyperammonemia, but it also provides a mechanism for testing new therapeutic modalities for the treatment of hyperammonemic encephalopathy.
机译：实验证据表明氨会引起神经兴奋和癫痫发作。这与通常被认为是高氨血症性脑病的主要成分的全球中枢神经系统抑郁症的嗜睡，困惑和其他表现形成鲜明对比。现在大量数据表明，氨可以通过直接和间接机制调节GABA能神经传递。这种调节包括在高氨血症状态下通常遇到的浓度下增强GABA能神经传递，并先于在较高（> 1mM）氨浓度下抑制抑制性神经元功能。 GABA能神经传递的这种增加不仅与与肝衰竭和先天性高氨血症相关的嗜睡，共济失调和认知缺陷的临床表现相符，而且还提供了一种机制，用于测试治疗高氨性脑病的新疗法。

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