Neuron-Glia Crosstalk in the Autonomic Nervous System and Its Possible Role in the Progression of Metabolic Syndrome: A New Hypothesis.
Neuron-Glia Crosstalk in the Autonomic Nervous System and Its Possible Role in the Progression of Metabolic Syndrome: A New Hypothesis.
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DOI：
10.3389/fphys.2015.00350
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发表时间：
2015
影响因子：
4
通讯作者：
Retamal MA
中科院分区：
文献类型：
--
作者：
Del Rio R;Quintanilla RA;Orellana JA;Retamal MA
代谢综合征（MS）以以下生理改变为特征：腹部脂肪增加、胰岛素抵抗、甘油三酯浓度高、高密度脂蛋白水平低、高血压和全身性炎症状态。该综合征的病理生理特征之一是存在神经体液激活，这涉及与交感神经系统过度激活相关的自主神经失衡。事实上，交感神经驱动的增强与内皮功能障碍、高血压、中风、心肌梗死和阻塞性睡眠呼吸暂停的发生有关。神经胶质细胞是中枢神经系统中数量最多的细胞，通过释放被称为神经胶质递质的生物活性分子来控制突触传递并调节神经元功能。最近，一种被称为半通道的新质膜通道家族被描述为允许胶质递质的释放和调节神经元放电速率。此外，越来越多的证据表明，不受控制的半通道开放可能损害神经胶质细胞功能，影响突触传递和神经元存活。鉴于胶质细胞功能在各种代谢性疾病中受到干扰，我们假设MS的进展可能依赖于胶质细胞与神经元间通讯的半通道依赖性损伤，其机制与胶质细胞的炎症反应和线粒体代谢功能障碍有关。在这篇文章中，我们讨论了神经胶质细胞如何促进在MS中观察到的增强的交感神经驱动，并阐明了半通道在这一过程中的可能作用。
Metabolic syndrome (MS) is characterized by the following physiological alterations: increase in abdominal fat, insulin resistance, high concentration of triglycerides, low levels of HDL, high blood pressure, and a generalized inflammatory state. One of the pathophysiological hallmarks of this syndrome is the presence of neurohumoral activation, which involve autonomic imbalance associated to hyperactivation of the sympathetic nervous system. Indeed, enhanced sympathetic drive has been linked to the development of endothelial dysfunction, hypertension, stroke, myocardial infarct, and obstructive sleep apnea. Glial cells, the most abundant cells in the central nervous system, control synaptic transmission, and regulate neuronal function by releasing bioactive molecules called gliotransmitters. Recently, a new family of plasma membrane channels called hemichannels has been described to allow the release of gliotransmitters and modulate neuronal firing rate. Moreover, a growing amount of evidence indicates that uncontrolled hemichannel opening could impair glial cell functions, affecting synaptic transmission and neuronal survival. Given that glial cell functions are disturbed in various metabolic diseases, we hypothesize that progression of MS may relies on hemichannel-dependent impairment of glial-to-neuron communication by a mechanism related to dysfunction of inflammatory response and mitochondrial metabolism of glial cells. In this manuscript, we discuss how glial cells may contribute to the enhanced sympathetic drive observed in MS, and shed light about the possible role of hemichannels in this process.