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首页> 外文期刊>The European Journal of Neuroscience >Coincident pre- and postsynaptic activity downregulates NKCC1 to hyperpolarize E(Cl) during development.
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Coincident pre- and postsynaptic activity downregulates NKCC1 to hyperpolarize E(Cl) during development.

机译：巧合的突触前和突触后活动下调NKCC1在发育过程中使E（Cl）超极化。

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摘要

In the mature CNS, coincident pre- and postsynaptic activity decreases the strength of gamma-aminobutyric acid (GABA)(A)-mediated inhibition through a Ca2+-dependent decrease in the activity of the neuron-specific K+-Cl- cotransporter KCC2. In the present study we examined whether coincident pre- and postsynaptic activity can also modulate immature GABAergic synapses, where the Na+-K+-2Cl- (NKCC1) cotransporter maintains a relatively high level of intracellular chloride ([Cl-](i)). Dual perforated patch-clamp recordings were made from cultured hippocampal neurons prepared from embryonic Sprague-Dawley rats. These recordings were used to identify GABAergic synapses where the reversal potential for Cl- (ECl) was hyperpolarized with respect to the action potential threshold but depolarized with respect to the resting membrane potential. At these synapses, repetitive postsynaptic spiking within +/- 5 ms of GABAergic synaptic transmission resulted in a hyperpolarizing shift of ECl by 10.03 +/- 1.64 mV, increasing the strength of synaptic inhibition. Blocking the inward transport of Cl- by NKCC1 with bumetanide (10 microm) hyperpolarized ECl by 16.14 +/- 4.8 mV, and prevented this coincident activity-induced shift of ECl. The bumetanide-induced hyperpolarization of ECl occluded furosemide, a K+-Cl- cotransporter antagonist, from producing further shifts in ECl. Together, this indicates that brief coincident pre- and postsynaptic activity strengthens inhibition through a regulation of NKCC1. This study further demonstrates ionic plasticity as a mechanism underlying inhibitory synaptic plasticity.
机译：在成熟的中枢神经系统中，同时的突触前和突触后活性通过神经元特异性K + -Cl-共转运蛋白KCC2的Ca2 +依赖性降低而降低了γ-氨基丁酸（GABA）（A）介导的抑制作用。在本研究中，我们研究了突触前和突触后活动是否同时还能调节未成熟的GABA能突触，其中Na + -K + -2Cl-（NKCC1）协同转运蛋白维持较高水平的细胞内氯化物（[Cl-]（i））。从胚胎Sprague-Dawley大鼠制备的培养的海马神经元制作了双孔膜片钳记录。这些记录用于鉴定GABA能突触，其中C1-（EC1）的逆转电位相对于动作电位阈值是超极化的，而相对于静息膜电位是去极化的。在这些突触处，在GABA能突触传递的+/- 5 ms内重复的突触后突刺导致EC1的超极化移位了10.03 +/- 1.64 mV，从而增加了突触抑制的强度。用布美他尼（10微米）超极化ECl阻止NKCC1向Cl-的向内运输，阻止了16.14 +/- 4.8 mV的ECl迁移，并阻止了此活动引起的ECl的同时迁移。布美他尼诱导的ECI超极化使速尿（一种K + -Cl-转运蛋白拮抗剂）闭塞，导致ECl发生进一步的变化。在一起，这表明短暂的同时突触前和突触后活动通过调节NKCC1增强了抑制作用。这项研究进一步证明了离子可塑性是抑制突触可塑性的基础机制。

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