锂调节脱敏的谷氨酸受体亚型gluR3非洲爪蟾蜍卵母细胞。
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Karkanias NB, Papke RL
锂调节脱敏的谷氨酸受体亚型gluR3非洲爪蟾蜍卵母细胞。
>。1999年12月31日,277 (3):153 - 6。
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10626836 (在PubMed]
- 文摘
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分析接头的变异和基因定点突变体AMPA受体GluR3表达非洲爪蟾蜍卵母细胞表明锂产生很大的增强作用GluR3失败拼接变体和建议锂可能抑制快速脱敏,这种受体的特征(Karkanias: Papke, R。,Subtype-specific锂对谷氨酸受体功能的影响。j . Neurophysiol。81 (1999)1506 - 1512)。我们现在表明,突变的769 r / G脱敏网站(Lomeli H.M.J.梅尔彻,T。猪,T。盖革,jr库恩,T。许多的,H。Higuchi mba和Seeburg, P。H,控制AMPA受体通道的动力学性质的核RNA编辑。科学、9(266)(1994)1709 - 1713)大大减弱lithium-induced GluR3的强化。此外,实验non-desensitizing定点突变GluR3 (L507Y) (Stern-Bach Y。罗威S。, Neuman, M. and Rosenmund, C., A point mutation in the glutamate binding site blocks desensitization of AMPA receptors. Neuron, 21 (1998) 907-918) further confirms that lithium enhances GluR3 responses by reducing desensitization, since lithium's effects are reversed in this mutant. Lithium's effects on GluR3 desensitization are distinct from the effects of aniracetam on desensitization. Specifically, aniracetam, which potentiates wild-type AMPA receptors, is ineffective on the non-desensitizing GluR3(L507Y) mutant, but has synergistic effects with lithium on wild-type receptors.