突触前HCN通道调节囊泡谷氨酸转运。
Presynaptic HCN channels regulate vesicular glutamate transport.
作者信息
Huang Hai, Trussell Laurence O
机构信息
Oregon Hearing Research Center & Vollum Institute, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, L335A, Portland, OR 97239, USA; Department of Cell and Molecular Biology, Tulane University, 2000 Percival Stern Hall, 6400 Freret Street, New Orleans, LA 70118, USA.
Oregon Hearing Research Center & Vollum Institute, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, L335A, Portland, OR 97239, USA.
出版信息
Neuron. 2014 Oct 22;84(2):340-6. doi: 10.1016/j.neuron.2014.08.046. Epub 2014 Sep 25.
The amount of neurotransmitter stored in synaptic vesicles determines postsynaptic quantal size and thus the strength of synaptic transmission. However, little is known about regulation of vesicular neurotransmitter uptake. In recordings from the calyx of Held, a giant mammalian glutamatergic synapse, we found that changes in presynaptic Na(+) concentration above and below a resting value of 13 mM regulated vesicular glutamate uptake, consistent with activation of a vesicular monovalent cation Na(+)(K(+))/H(+) exchanger. Na(+) flux through presynaptic plasma membrane hyperpolarization-activated cyclic nucleotide-gated (HCN) channels enhanced presynaptic Na(+) concentration and thus controlled postsynaptic quantal size. Our results indicate that a plasma membrane ion channel controls synaptic strength by modulating vesicular neurotransmitter uptake through a Na(+)-dependent process.
储存在突触小泡中的神经递质数量决定了突触后量子大小，进而决定了突触传递的强度。然而，关于小泡神经递质摄取的调节却知之甚少。在对Held壶腹（一种巨大的哺乳动物谷氨酸能突触）的记录中，我们发现，突触前Na⁺浓度在13 mM的静息值上下发生变化时，会调节小泡谷氨酸摄取，这与小泡单价阳离子Na⁺(K⁺)/H⁺交换体的激活相一致。通过突触前质膜超极化激活的环核苷酸门控（HCN）通道的Na⁺通量会提高突触前Na⁺浓度，从而控制突触后量子大小。我们的结果表明，质膜离子通道通过一个依赖Na⁺的过程调节小泡神经递质摄取，从而控制突触强度。
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