beta-adrenergic stimulation promotes homocysteic acid release from astrocyte cultures: Evidence for a role of astrocytes in the modulation of synaptic transmission
beta-adrenergic stimulation promotes homocysteic acid release from astrocyte cultures: Evidence for a role of astrocytes in the modulation of synaptic transmission
复制标题
β-肾上腺素能刺激可促进星形胶质细胞培养物释放同型半胱氨酸： 星形胶质细胞在调节突触传递中发挥作用的证据
DOI：
10.1046/j.1471-4159.1997.68062386.x
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发表时间：
1997-06-01
影响因子：
4.7
通讯作者：
Magistretti, PJ
中科院分区：
文献类型：
--
作者：
Do, KQ;Benz, B;Magistretti, PJ
含硫氨基酸同型半胱氨酸（HCA）存在于神经组织中并从神经组织释放，主要通过激活NMDA受体对神经元产生兴奋作用。有趣的是，HCA似乎只局限于神经胶质细胞，而不是神经元。这种神经胶质的定位和对神经元的兴奋作用的特征导致了HCA可能作为“胶质传递物”参与脑中细胞间通讯的假设。为了进一步验证这一假设，我们寻找特异的受体介导的刺激物，可以诱导培养的星形胶质细胞释放HCA。出于这个原因，我们测试了去甲肾上腺素和血管活性肠肽（已知与星形胶质细胞上的特异性受体相互作用的两种递质）对这些细胞释放HCA的影响。去甲肾上腺素和β-肾上腺素能激动剂异丙肾上腺素诱导HCA从星形胶质细胞培养物中流出。阿替洛尔阻断异丙肾上腺素引起的HCA释放，进一步强调了β-肾上腺素能介导的这种作用。用α-去甲肾上腺素能激动剂甲氧胺和血管活性肠肽未观察到HCA从星形胶质细胞释放的刺激。这些结果加在一起进一步加强了HCA作为胶质递质的作用。它从胶质细胞的流出可以由去甲肾上腺素控制，激活星形胶质细胞上的β-肾上腺素能受体。本研究提供了第一个证据β-肾上腺素能受体激活对星形胶质细胞释放兴奋性氨基酸的影响，并进一步支持神经胶质细胞-神经元相互作用在突触传递中发挥作用的观点。
The sulfur-containing amino acid homocysteic acid (HCA) is present in and released from nervous tissue, exerting excitatory effects on neurons by predominantly activating NMDA receptors. It is interesting that HCA appears to be exclusively localized in glial cells, not in neurons. This profile of glial localization and excitatory action on neurons has led to the hypothesis that HCA could participate in intercellular communication in the brain as a ''gliotransmitter.'' To test this hypothesis further, we searched for specific, receptor-mediated stimuli that could induce release of HCA from cultured astrocytes. For this reason we tested the effect of noradrenaline and vasoactive intestinal peptide, two transmitters known to interact with specific receptors on astrocytes, on the release of HCA from these cells. Noradrenaline and the beta-adrenergic agonist isoproterenol induced an efflux of HCA from astrocyte cultures. Further stressing the beta-adrenergic mediation of this effect is the blockade by atenolol of the HCA release evoked by isoproterenol. The stimulation of HCA release from astrocytes was not observed with the alpha-noradrenergic agonist methoxamine and with vasoactive intestinal peptide. These results taken together further strengthen the role of HCA as a gliotransmitter. Its efflux from glia could be controlled by noradrenaline, activating beta-adrenergic receptors on astrocytes. The present study provides the first evidence for an influence of beta-adrenergic receptor activation on the release of an excitatory amino acid from astrocytes and further supports the notion that glial-neuronal interactions play a role in synaptic transmission.