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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >G protein-dependent presynaptic inhibition mediated by AMPA receptors at the calyx of Held
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G protein-dependent presynaptic inhibition mediated by AMPA receptors at the calyx of Held

机译：在Held的花萼中由AMPA受体介导的G蛋白依赖性突触前抑制

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摘要

The α-amino-3-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) is an ionotropic receptor mediating excitatory synaptic transmission, but it can also interact with intracellular messengers. Here we report that, at the calyx of Held in the rat auditory brainstem, activation of AMPARs induced inward currents in the nerve terminal and inhibited presynaptic Ca~(2+) currents (I_(pCa)). thereby attenuating glutamatergic synaptic transmission. The AM-PAR-mediated I_(pCa) inhibition was disinhibited by a strong depolarizing pulse and occluded by the nonhydrolyzable GTP analog GTPγS loaded into the terminal. We conclude that functional AMPARs are expressed at the calyx of Held nerve terminal and that their activation inhibits voltage-gated Ca~(2+) channels by an interaction with heterotrimeric GTP-binding proteins (G proteins). Thus, at a central glutamatergic synapse, presynaptic AMPARs have a metabotropic nature and regulate transmitter release by means of G proteins.
机译：α-氨基-3-5-甲基-4-异恶唑丙酸受体（AMPAR）是介导兴奋性突触传递的离子型受体，但它也可以与细胞内信使相互作用。在这里，我们报告说，在大鼠听觉脑干Held的花萼中，AMPAR的激活在神经末梢诱导了内向电流，并抑制了突触前Ca〜（2+）电流（I_（pCa））。从而减弱谷氨酸能突触传递。 AM-PAR介导的I_（pCa）抑制作用被强去极化脉冲抑制，并被装载在末端的不可水解GTP类似物GTPγS所阻塞。我们得出结论，功能性AMPARs在被握神经末梢的花萼中表达，其激活通过与异三聚体GTP结合蛋白（G蛋白）的相互作用抑制电压门控的Ca〜（2+）通道。因此，在中央谷氨酸能突触处，突触前AMPAR具有亲代谢性质并通过G蛋白调节递质释放。

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