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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 >Effect of ammonia on GABA uptake and release in cultured astrocytes.
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Effect of ammonia on GABA uptake and release in cultured astrocytes.

机译：氨对培养的星形胶质细胞中GABA吸收和释放的影响。

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摘要

While the pathogenesis of hepatic encephalopathy (HE) is unclear, there is evidence of enhanced GABAergic neurotransmission in this condition. Ammonia is believed to play a major pathogenetic role in HE. To determine whether ammonia might contribute to abnormalities in GABAergic neurotransmission, its effects on GABA uptake and release were studied in cultured astrocytes, cells that appear to be targets of ammonia neurotoxicity. Acutely, ammonium chloride (5 mM) inhibited GABA uptake by 30%, and by 50-60% after 4-day treatment. GABA uptake inhibition was associated with a predominant decrease in Vmax; the Km was also decreased. Ammonia also enhanced GABA release after 4-day treatment, although such release was initially inhibited. These effects of ammonia (inhibition of GABA uptake and enhanced GABA release) may elevate extracellular levels of GABA and contribute to a dysfunction of GABAergic neurotransmission in HE and other hyperammonemic states.
机译：虽然尚不清楚肝性脑病（HE）的发病机理，但有证据表明这种情况下GABA能神经传递增强。氨被认为在HE中起主要的致病作用。为了确定氨是否可能导致GABA能神经传递异常，在培养的星形胶质细胞中研究了其对GABA吸收和释放的影响，星形胶质细胞似乎是氨神经毒性的靶标。急性氯化铵（5 mM）抑制GABA摄取30％，治疗4天后抑制50-60％。 GABA的摄取抑制与Vmax的显着降低有关。 Km也降低了。氨还增强了4天处理后GABA的释放，尽管这种释放最初受到抑制。氨的这些作用（抑制GABA摄取和增强GABA释放）可能会升高细胞外GABA水平，并导致HE和其他高氨血症状态下GABA能神经传递功能障碍。

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