Glutamate release monitored with astrocyte transporter currents during LTP
Glutamate release monitored with astrocyte transporter currents during LTP
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DOI：
10.1016/s0896-6273(00)80551-6
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发表时间：
1998-08-01
期刊：
影响因子：
16.2
通讯作者：
Jahr, CE
中科院分区：
文献类型：
--
作者：
Diamond, JS;Bergles, DE;Jahr, CE
海马CA 1区突触传递的长时程增强（LTP）被认为是由递质释放增加、突触后敏感性增强或两者结合引起的。我们已经测量了诱发谷氨酸释放谢弗侧支/连合纤维终端在CA 1通过记录突触激活谷氨酸转运体电流位于辐射层的海马星形胶质细胞。虽然释放概率的几个操作引起细胞外场电位和突触激活的转运体电流幅度的平行变化，LTP的诱导未能改变转运体介导的反应，表明LTP不改变突触刺激后释放的谷氨酸的量。
Long-term potentiation (LTP) of synaptic transmission in the CA1 region of the hippocampus is thought to result from either increased transmitter release, heightened postsynaptic sensitivity, or a combination of the two. We have measured evoked glutamate release from Schaffer collateral/commissural fiber terminals in CA1 by recording synaptically activated glutamate transporter currents in hippocampal astrocytes located in stratum radiatum. Although several manipulations of release probability caused parallel changes in extracellular field potentials and synaptically activated transporter current amplitudes, induction of LTP failed to alter transporter-mediated responses, suggesting that LTP does not alter the amount of glutamate released upon synaptic stimulation.