A novel neurotransmitter-independent communication pathway between axons and glial cells
A novel neurotransmitter-independent communication pathway between axons and glial cells
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DOI：
10.1111/j.1460-9568.2007.05351.x
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发表时间：
2007-02-01
影响因子：
3.4
通讯作者：
Lohr, Christian
中科院分区：
文献类型：
--
作者：
Hartl, Sandra;Heil, Jan E.;Lohr, Christian
最近的研究提供的证据表明，神经元释放的递质可以激活神经胶质受体并刺激神经胶质细胞中的钙信号传导。胶质细胞钙信号转导反过来可能会影响神经元的性能，例如突触功效的长期变化。嗅鞘细胞（OEC）是脊椎动物和昆虫中的一种特殊神经胶质细胞类型，促进发育和成熟神经系统中的轴突生长。然而，迄今为止，OEC 的生理特性尚未得到详细研究。我们测量了天蛾 Manduca sexta 的 OEC 中钙浓度的原位和体内变化。对蛹中嗅觉受体神经元的电刺激或对成虫中受体神经元的气味刺激会导致 OEC 中的钙瞬变。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（例如谷氨酸、GABA 或一氧化氮）不会在 OEC 中诱导钙瞬变。神经刺激后，用钾敏感微电极测量，细胞外钾升高了几毫摩尔。当灌注盐水中的钾从 4 mM 增加到 10 mM 或更高时，OEC 中会引起类似于刺激诱导的钙瞬变的电压依赖性钙瞬变。用 TEA 阻断神经元钾通道可减少刺激引起的细胞外钾增加和 OEC 中的钙瞬变，而受体轴突中的钙瞬变则增加。我们的结果首次表明，电活性轴突释放的钾积累足以引起电压依赖性钙流入神经胶质细胞，而神经递质似乎不参与天蛾的这种神经元-神经胶质细胞通讯。
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.