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首页> 外文期刊>Journal of Neurophysiology >Intrinsic and synaptic homeostatic plasticity in motoneurons from mice with glycine receptor mutations
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Intrinsic and synaptic homeostatic plasticity in motoneurons from mice with glycine receptor mutations

机译：用甘氨酸受体突变小鼠的运动神经元的内在和突触稳态可塑性

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Inhibitory synaptic inputs to hy-poglossal motoneurons (HMs) are important for modulating excitability in brainstem circuits. Here we ask whether reduced inhibition, as occurs in three murine mutants with distinct naturally occurring mutations in the glycine receptor (GlyR), leads to intrinsic and/or synaptic homeostatic plasticity. Whole cell recordings were obtained from HMs in transverse brainstem slices from wild-type (wt), spasmodic (spd), spastic (spa), and oscillator (of) mice (C57B1/6, approximately postnatal day 21). Passive and action potential (AP) properties in spd and ot HMs were similar to wt. In contrast, spa HMs had lower input resistances, more depolarized resting membrane potentials, higher rheobase currents, smaller AP amplitudes, and slower afterhy-perpolarization current decay times. The excitability of HMs, assessed by "gain" in injected current/firing-frequency plots, was similar in all strains whereas the incidence of rebound spiking was increased in spd. The difference between recruitment and derecruitment current (i.e., A/) for AP discharge during ramp current injection was more negative in spa and ot. GABA_A miniature inhibitory postsynaptic current (mlPSC) amplitude was increased in spa and ot but not spd, suggesting diminished glycinergic drive leads to compensatory adjustments in the other major fast inhibitory synaptic transmitter system in these mutants. Overall, our data suggest long-term reduction in glycinergic drive to HMs results in changes in intrinsic and synaptic properties that are consistent with homeostatic plasticity in spa and ot but not in spd. We propose such plasticity is an attempt to stabilize HM output, which succeeds in spa but fails in ot.
机译：对Hy-Poglossal运动神经元（HMS）的抑制突触输入对于调节脑干电路中的兴奋是重要的。在这里，我们询问是否在甘氨酸受体（GLYR）中具有不同天然存在的突变的三个鼠突变体中的减少抑制，导致内在和/或突触稳态可塑性。从野生型（WT），痉挛（SPD），痉挛（SPA），痉挛（SPA）和振荡器（OF）小鼠（C57B1 / 6，大约后第21天）中从横向脑干切片中获得全部细胞录音。 SPD和OT HMS中的被动和动作潜力（AP）属性类似于WT。相反，SPA HMS具有较低的输入抗性，更差极化的静止膜电位，更高的Rheobase电流，更小的AP振幅，以及较慢的后半系化电流衰减时间。通过“增益”在注入的电流/烧制频率图中评估的HMS的兴奋性在所有菌株中相似，而反弹尖峰的发生率在SPD中增加。在斜坡电流注射期间AP放电的招生和遗漏电流（即A /）之间的差异在水疗中心和OT中更为阴性。 SPA和OT的GABA_A微型抑制后突触电流（MLPSC）振幅增加，但不是SPD，表明甘油能驱动减少导致这些突变体中的其他主要快速抑制突触变送器系统中的补偿调整。总体而言，我们的数据表明甘氨酸能量的长期减少到HMS导致内在和突触特性的变化，其与SPA和OT中的稳态可塑性一致，但不是在SPD中。我们提出这种可塑性是试图稳定HM输出，其在SPA中成功，但在OT中失败。

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