神经配体诱发雪旺细胞中兴奋性氨基酸的钙依赖性释放。
Neuroligand-evoked calcium-dependent release of excitatory amino acids from Schwann cells.
作者信息
Parpura V, Liu F, Jeftinija K V, Haydon P G, Jeftinija S D
机构信息
Department of Zoology and Genetics, Iowa State University, Ames 50011, USA.
出版信息
J Neurosci. 1995 Aug;15(8):5831-9. doi: 10.1523/JNEUROSCI.15-08-05831.1995.
Bradykinin caused a receptor-mediated increase in release of the excitatory amino acids (EAAs) glutamate and aspartate from Schwann cell cultures obtained from dorsal root ganglia (DRG) together with an increase in the cytoplasmic level of free calcium. Perturbations which inhibited brady-kinin-induced calcium mobilization prevented the release of EAAs from glia. The addition of ionomycin caused a calcium-dependent release of EAAs. Therefore, bradykinin causes calcium dependent-release of EAAs from DRG Schwann cells. Bradykinin did not cause cell swelling and p-chloromercuriphenylsulfonic acid, an inhibitor of the electrogenic glutamate transporter, did not reduce bradykinin-induced EAA release. Therefore, bradykinin stimulates EAA release from Schwann cells through a mechanism that is neither the previously described volume regulated release mechanism nor due to the reversal of the glutamate transporter.
缓激肽可引起受体介导的兴奋性氨基酸（EAAs）谷氨酸和天冬氨酸从背根神经节（DRG）雪旺细胞培养物中的释放增加，同时细胞内游离钙水平升高。抑制缓激肽诱导的钙动员的干扰因素可阻止胶质细胞释放EAAs。添加离子霉素可引起EAAs的钙依赖性释放。因此，缓激肽可引起DRG雪旺细胞钙依赖性释放EAAs。缓激肽不会导致细胞肿胀，而电生性谷氨酸转运体抑制剂对氯汞苯磺酸也不会减少缓激肽诱导的EAA释放。因此，缓激肽通过一种既不是先前描述的容量调节释放机制，也不是由于谷氨酸转运体逆转的机制刺激雪旺细胞释放EAA。
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