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在长时程增强期间,通过星形胶质细胞转运体电流监测谷氨酸释放。

Glutamate release monitored with astrocyte transporter currents during LTP.

作者信息

Diamond J S, Bergles D E, Jahr C E

机构信息

Vollum Institute, Oregon Health Sciences University, Portland 97201, USA.

出版信息

Neuron. 1998 Aug;21(2):425-33. doi: 10.1016/s0896-6273(00)80551-6.

Abstract

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.

摘要

海马体CA1区突触传递的长时程增强(LTP)被认为是由递质释放增加、突触后敏感性提高或两者共同作用所致。我们通过记录位于辐射层的海马星形胶质细胞中突触激活的谷氨酸转运体电流,测量了CA1区Schaffer侧支/联合纤维终末诱发的谷氨酸释放。尽管对释放概率的几种操作导致细胞外场电位和突触激活的转运体电流幅度发生平行变化,但LTP的诱导未能改变转运体介导的反应,这表明LTP不会改变突触刺激时释放的谷氨酸量。

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