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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：具有甘氨酸受体突变的小鼠运动神经元的内在和突触体内稳态可塑性

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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：舌下运动神经元（HMs）的抑制性突触输入对于调节脑干回路的兴奋性很重要。在这里，我们要问抑制的抑制作用是否降低，如在甘氨酸受体（GlyR）中具有明显不同的天然突变的三个鼠类突变体中所发生的抑制作用，是否导致内在的和/或突触的稳态可塑性。从野生型（wt），痉挛性（spd），痉挛性（spa）和振动子（of）小鼠（C57B1 / 6，大约在出生后第21天）的横向脑干切片中的HM获得全细胞记录。 spd和ot HM的被动和动作电位（AP）特性与wt。相反，spa HM具有更低的输入电阻，更多的去极化静息膜电位，更高的流变碱电流，更小的AP振幅以及较慢的超极化后电流衰减时间。在所有菌株中，通过注入电流/发射频率图中的“增益”评估的HMs的兴奋性在所有菌株中均相似，而在spd中反弹尖峰的发生率却有所增加。在spa和ot中，在斜坡电流注入期间AP放电的募集和撤消电流（即A /）之间的差异更大。在spa和ot中GABA_A微型抑制性突触后电流（mlPSC）幅度增加，但spd没有增加，这表明这些变量中甘氨酸驱动力降低导致其他主要的快速抑制性突触递质系统发生补偿性调节。总体而言，我们的数据表明，对HM的甘氨酸驱动力的长期减少会导致内在和突触特性的变化，这与spa和ot的稳态可塑性一致，但在spd中却没有。我们建议这种可塑性是稳定HM输出的尝试，这种方法在spa中成功但在ot中失败。

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