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轴突与神经胶质细胞之间一种新型的非神经递质依赖的通讯途径。

A novel neurotransmitter-independent communication pathway between axons and glial cells.

作者信息

Hartl Sandra, Heil Jan E, Hirsekorn Andrea, Lohr Christian

机构信息

Abteilung für Allgemeine Zoologie, T. U. Kaiserslautern, PO Box 3049, 67653 Kaiserslautern, Germany.

出版信息

Eur J Neurosci. 2007 Feb;25(4):945-56. doi: 10.1111/j.1460-9568.2007.05351.x.

DOI:10.1111/j.1460-9568.2007.05351.x
PMID:17331192
Abstract

Recent studies have provided evidence that transmitters released by neurons can activate glial receptors and stimulate calcium signalling in glial cells. Glial calcium signalling, in turn, may affect neuronal performance such as long-term changes in synaptic efficacy. Olfactory ensheathing cells (OECs) are a special glial cell type in vertebrates and insects and promote axon growth in the developing and mature nervous system. Physiological properties of OECs, however, have not been studied so far in detail. We measured changes in the calcium concentration in OECs of the moth Manduca sexta, in situ and in vivo. Electrical stimulation of olfactory receptor neurons in pupae or odour stimulation of receptor neurons in adults resulted in calcium transients in OECs. Olfactory receptor axons release acetylcholine; however, application of acetylcholine or other transmitters such as glutamate, GABA or nitric oxide did not induce calcium transients in OECs. Upon nerve stimulation, extracellular potassium rose by several millimolar as measured with potassium-sensitive microelectrodes. When potassium in the perfusion saline was increased from 4 to 10 mM or higher, voltage-dependent calcium transients in OECs that resembled stimulation-induced calcium transients were evoked. Blocking neuronal potassium channels with TEA reduced both the stimulation-induced increases in extracellular potassium and the calcium transients in OECs, whereas calcium transients in receptor axons were augmented. Our results show for the first time that accumulation of potassium, released by electrically active axons, is sufficient to evoke voltage-dependent calcium influx into glial cells, whereas neurotransmitters appear not to be involved in this neuron-glia communication in Manduca.

摘要

最近的研究已提供证据表明,神经元释放的递质可激活胶质细胞受体并刺激胶质细胞中的钙信号传导。反过来,胶质细胞的钙信号传导可能会影响神经元的功能,如突触效能的长期变化。嗅鞘细胞(OECs)是脊椎动物和昆虫中的一种特殊胶质细胞类型,在发育中和成熟的神经系统中促进轴突生长。然而,迄今为止尚未对OECs的生理特性进行详细研究。我们在原位和体内测量了烟草天蛾OECs中钙浓度的变化。对蛹期的嗅觉受体神经元进行电刺激或对成虫的受体神经元进行气味刺激,均导致OECs中出现钙瞬变。嗅觉受体轴突释放乙酰胆碱;然而,应用乙酰胆碱或其他递质,如谷氨酸、γ-氨基丁酸或一氧化氮,并未在OECs中诱导钙瞬变。通过神经刺激,用钾敏感微电极测量发现细胞外钾升高了数毫摩尔。当灌注盐水中的钾从4 mM增加到10 mM或更高时,OECs中出现了类似于刺激诱导的钙瞬变的电压依赖性钙瞬变。用四乙铵(TEA)阻断神经元钾通道,可降低刺激诱导的细胞外钾升高以及OECs中的钙瞬变,而受体轴突中的钙瞬变则增强。我们的结果首次表明,电活动轴突释放的钾的积累足以引起电压依赖性钙流入胶质细胞,而在烟草天蛾中,神经递质似乎不参与这种神经元与胶质细胞之间的通讯。

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