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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 >GABA and NMDA in the prevention of apoptotic-like cell death in vitro.
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GABA and NMDA in the prevention of apoptotic-like cell death in vitro.

机译：GABA和NMDA在体外预防凋亡样细胞死亡。

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We have shown recently that cerebellar granule neurons die in the absence of depolarizing concentrations of KCl through an apoptosis-like process. To study the contributions of inhibitory (gamma-aminobutyric acid; GABA) and excitatory (glutamate) neurotransmitters in the prevention of apoptotic-like cell death in cultures grown in the presence of reduced concentrations of KCl (12.5 mM), we treated these cultures either acutely or chronically with GABA, bicuculline methiodide, a GABAA receptor antagonist, N-methyl-D-aspartate (NMDA) and/or the NMDA receptor antagonist, MK-801. Cell viability was measured with fluorescein diacetate/propidium iodide (FDA/PI) and trypan blue exclusion tests. In addition, DNA fragmentation was assessed quantitatively using an in situ terminal deoxynucleotidyl transferase assay. Our results demonstrate that treatment of cerebellar granule cell cultures maintained in 12.5 mM KCl with the glutamate receptor agonist NMDA and/or bicuculline protects against cell death and reduces DNA fragmentation. In contrast, GABA potentiated cerebellar granule cell apoptosis mediated by KCl deprivation. These data indicate that signal transduction pathways activated following NMDA receptor stimulation mimic the anti-apoptotic action of high potassium in primary cultures of cerebellar granule neurons. Also, our data support an inhibitory (hyperpolarizing) role for GABA in these cultures. Collectively, the results suggest that the neurotrophic actions of NMDA on granule cells maintained in low KCl and GABA on granule cells cultured in high KCl are due to the necessity for maintaining appropriate intraneuronal calcium concentrations.
机译：我们最近显示，小脑颗粒神经元在无去极化浓度的KCl通过凋亡样过程死亡。为了研究抑制性（γ-氨基丁酸; GABA）和兴奋性（谷氨酸）神经递质在预防KCl（12.5 mM）浓度降低的培养物中凋亡样细胞死亡中的作用，我们对这些培养物进行了处理急性或慢性与GABA，双环甲硫氨酸，一种GABAA受体拮抗剂，N-甲基-D-天冬氨酸（NMDA）和/或NMDA受体拮抗剂MK-801联合使用。用二乙酸荧光素/碘化丙啶（FDA / PI）和台盼蓝排除试验测量细胞活力。另外，使用原位末端脱氧核苷酸转移酶测定法定量评估DNA片段化。我们的结果表明，用谷氨酸受体激动剂NMDA和/或双瓜氨酸处理维持在12.5 mM KCl中的小脑颗粒细胞培养物可防止细胞死亡并减少DNA断裂。相反，GABA增强了KCl剥夺介导的小脑颗粒细胞凋亡。这些数据表明，NMDA受体刺激后激活的信号转导通路模拟了小脑颗粒神经元原代培养物中高钾的抗凋亡作用。同样，我们的数据支持这些文化中GABA的抑制作用（超极化）。总的来说，该结果表明NMDA对维持在低KCl中的颗粒细胞的神经营养作用和GABA对维持在高KCl中的颗粒细胞的神经营养作用是由于必须保持适当的神经内钙浓度。

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