首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Dependence of long-term depression on postsynaptic metabotropic glutamate receptors in visual cortex.
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Dependence of long-term depression on postsynaptic metabotropic glutamate receptors in visual cortex.

机译:视觉皮层中长期抑制对突触后代谢型谷氨酸受体的依赖性。

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摘要

Long-term depression (LTD) is held relevant to memory and learning. Its induction is known to require postsynaptic calcium increases. However, the source of these calcium increases remains unclear. In visual cortex slices, LTD was induced by tetanization after blockade of N-methyl-D-aspartate (NMDA) and non-NMDA ionotropic glutamate receptors. LTD induced under this condition was prevented by an intracellular injection of each of the following drugs into the postsynaptic neuron: (i) guanosine 5'-[beta-thio]diphosphate, which competitively inhibits the binding of GTP to GTP-binding regulatory proteins; (ii) heparin, which antagonizes 1,4,5-inositol triphosphate binding; and (iii) calcium chelators. Moreover, LTD was induced without tetanization by applying quisqualate (10 microM), a metabotropic glutamate receptor agonist, but not another agonist, trans-aminocyclopentane-1,3-dicarboxylic acid (10 microM). Together, these results suggest that activation of 1,4,5-inositol trisphosphate-linked subtypes of metabotropic glutamate receptor is responsible for the increase in postsynaptic calcium concentration, which results in homosynaptic LTD.
机译:长期抑郁症(LTD)与记忆和学习有关。已知其诱导需要突触后钙增加。但是,这些钙增加的来源仍不清楚。在视觉皮层切片中,N-甲基-D-天门冬氨酸(NMDA)和非NMDA离子型谷氨酸受体被阻断后,通过成膜作用诱导LTD。通过向突触后神经元胞内注射以下每种药物来防止在这种情况下诱导的LTD:(i)鸟苷5'-β-硫代二磷酸,它竞争性地抑制GTP与GTP结合的调节蛋白的结合; (ii)肝素,拮抗1,4,5-肌醇三磷酸结合; (iii)钙螯合剂。此外,通过应用代谢型谷氨酸受体激动剂喹喹啉(10 microM),而不使用另一种激动剂,反式-氨基环戊烷-1,3-二羧酸(10 microM),可以诱导LTD不会被破伤。总之,这些结果表明,代谢型谷氨酸受体的1,4,5-肌醇三磷酸连接的亚型的激活是导致突触后钙浓度增加的原因,这导致了突触型LTD。

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