GLUTAMATE-MEDIATED ASTROCYTE NEURON SIGNALING
GLUTAMATE-MEDIATED ASTROCYTE NEURON SIGNALING
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DOI：
10.1038/369744a0
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发表时间：
1994-06-30
期刊：
影响因子：
64.8
通讯作者：
HAYDON, PG
中科院分区：
文献类型：
--
作者：
PARPURA, V;BASARSKY, TA;HAYDON, PG
已知从神经元释放的神经递质向邻近神经元和神经胶质发出信号（1-3）。在这里，我们证明了一个额外的信号通路，其中谷氨酸从星形胶质细胞释放，并导致NMDA（N-甲基-D-天冬氨酸）受体介导的神经元钙的增加。内部钙升高和谷氨酸释放刺激神经配体缓激肽的应用培养的星形胶质细胞。星形胶质细胞内部钙离子的升高也足以诱导谷氨酸的释放。为了确定这是否会向神经元释放谷氨酸信号，我们研究了星形胶质细胞-神经元共培养物。缓激肽显着增加与星形胶质细胞共培养的神经元中的钙水平，但不是在孤立的神经元。谷氨酸受体拮抗剂D-2-氨基-5-膦酸戊酸和D-谷氨酰甘氨酸阻止缓激肽诱导的神经元钙升高。当单个星形胶质细胞被直接刺激以增加内部钙并释放谷氨酸时，邻近神经元的钙水平增加;这种增加可以被D-谷氨酰甘氨酸阻断。因此，星形胶质细胞通过谷氨酸的钙依赖性释放来调节神经元钙水平。-
NEUROTRANSMITTER released from neurons is known to signal to neighbouring neurons and glia(1-3). Here we demonstrate an additional signalling pathway in which glutamate is released from astrocytes and causes an NMDA (N-methyl-D-aspartate) receptor-mediated increase in neuronal calcium. Internal calcium was elevated and glutamate release stimulated by application of the neuroligand bradykinin to cultured astrocytes. Elevation of astrocyte internal calcium was also sufficient to induce glutamate release. To determine whether this released glutamate signals to neurons, we studied astrocyte-neuron co-cultures. Bradykinin significantly increased calcium levels in neurons co-cultured with astrocytes, but not in solitary neurons. The glutamate receptor antagonists D-2-amino-5-phosphonopentanoic acid and D-glutamylglycine prevented bradykinin-induced neuronal calcium elevation. When single astrocytes were directly stimulated to increase internal calcium and release glutamate, calcium levels of adjacent neurons were increased; this increase could be blocked by D-glutamyl-glycine. Thus, astrocytes regulate neuronal calcium levels through the calcium-dependent release of glutamate. -