pH modulation of glial glutamate transporters regulates synaptic transmission in the nucleus of the solitary tract.
pH modulation of glial glutamate transporters regulates synaptic transmission in the nucleus of the solitary tract.
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神经胶质谷氨酸转运蛋白的 pH 调节调节孤束核中的突触传递。
DOI：
10.1152/jn.01074.2012
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发表时间：
2013
影响因子：
2.5
通讯作者：
Martina,Marco
中科院分区：
文献类型：
--
作者：
Huda,Rafiq;McCrimmon,DonaldR;Martina,Marco
孤束核（NTS）是终止内脏感觉传入的主要部位，有助于动脉压、胃动力和呼吸等稳态调节。尽管人们对不同神经元群如何影响这些功能了解很多，但有关神经胶质细胞作用的信息仍然很少。在本文中，我们提出神经胶质细胞可能通过调节兴奋性神经传递来促进 NTS 功能。我们发现酸化（pH 7.0）通过抑制 K+ 选择性膜电流使 NTS 神经胶质细胞去极化。 NTS 神经胶质细胞还表现出电压敏感谷氨酸转运蛋白的功能表达，表明细胞外酸化通过损害神经胶质细胞谷氨酸摄取来调节突触传递。为了验证这一假设，我们通过重复刺激孤束（10 Hz 下 20 个脉冲）在 NTS 神经元中诱发谷氨酸能慢兴奋电位 (SEP)。这种 SEP 取决于重复刺激后谷氨酸的积累，因为它是通过用 dl-苏型-β-苄氧基天冬氨酸 (TBOA) 或神经胶质细胞特异性谷氨酸转运阻滞剂二氢红藻氨酸 (DHK) 阻断谷氨酸摄取而增强的。重要的是，细胞外酸化（pH 7.0）也增强了 SEP。这种效应似乎是通过去极化诱导的神经胶质转运蛋白活性抑制介导的，因为它被 TBOA 和 DHK 阻断。一致认为，pH 7.0 并没有直接改变 NTS 神经胶质细胞中天冬氨酸诱导的反应或突触前谷氨酸释放的特性。因此，神经胶质功能的酸化依赖性调节影响 NTS 内的突触传递。这些结果表明，神经胶质细胞通过将局部组织信号（例如 pH）与来自周围传入神经的突触输入相结合，在 NTS 中发挥调节作用。
The nucleus of the solitary tract (NTS) is the major site for termination of visceral sensory afferents contributing to homeostatic regulation of, for example, arterial pressure, gastric motility, and breathing. Whereas much is known about how different neuronal populations influence these functions, information about the role of glia remains scant. In this article, we propose that glia may contribute to NTS functions by modulating excitatory neurotransmission. We found that acidification (pH 7.0) depolarizes NTS glia by inhibiting K+-selective membrane currents. NTS glia also showed functional expression of voltage-sensitive glutamate transporters, suggesting that extracellular acidification regulates synaptic transmission by compromising glial glutamate uptake. To test this hypothesis, we evoked glutamatergic slow excitatory potentials (SEPs) in NTS neurons with repetitive stimulation (20 pulses at 10 Hz) of the solitary tract. This SEP depends on accumulation of glutamate following repetitive stimulation, since it was potentiated by blocking glutamate uptake withdl-threo-β-benzyloxyaspartic acid (TBOA) or a glia-specific glutamate transport blocker, dihydrokainate (DHK). Importantly, extracellular acidification (pH 7.0) also potentiated the SEP. This effect appeared to be mediated through a depolarization-induced inhibition of glial transporter activity, because it was occluded by TBOA and DHK. In agreement, pH 7.0 did not directly alterd-aspartate-induced responses in NTS glia or properties of presynaptic glutamate release. Thus acidification-dependent regulation of glial function affects synaptic transmission within the NTS. These results suggest that glia play a modulatory role in the NTS by integrating local tissue signals (such as pH) with synaptic inputs from peripheral afferents.
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