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N-甲基-D-天冬氨酸受体和电压依赖性钙通道参与吗啡依赖大鼠海马CA1区长时程增强的增强作用。

Involvement of NMDA receptors and voltage-dependent calcium channels on augmentation of long-term potentiation in hippocampal CA1 area of morphine dependent rats.

作者信息

Pourmotabbed A, Motamedi F, Fathollahi Y, Mansouri F A, Semnanian S

机构信息

Department of physiology, School of Medicine, Shaheed Beheshti University of Medical Sciences, P.O. Box 19835-181, Evin, Tehran, Iran.

出版信息

Brain Res. 1998 Aug 31;804(1):125-34. doi: 10.1016/s0006-8993(98)00676-3.

DOI:10.1016/s0006-8993(98)00676-3
PMID:9729327
Abstract

The involvement of NMDA receptors and voltage-dependent calcium channels on augmentation of long-term potentiation (LTP) was investigated at the Schaffer collateral-CA1 pyramidal cell synapses in hippocampal slices of morphine dependent rats, using primed-bursts tetanic stimulation. The amplitude of population spike was measured as an index of increase in postsynaptic excitability. d, l-AP5 and nifedipine were used as NMDA receptor antagonist and voltage-dependent calcium channel blocker, respectively. The amount of LTP of orthodromic population spike amplitude was higher in slices from dependent rats. Perfusion of slices from control or dependent rats with ACSF containing either D,L-AP5 (25 microM) or nifedipine (10 microM) and delivering tetanic stimulation, showed that D,L-AP5 completely blocked LTP of OPS in slices from both control and dependent rats, while nifedipine attenuated the amount of LTP of OPS in dependent slices and had no effect on control ones. The results suggest that the enhanced LTP of OPS in the CA1 area of hippocampal slices from morphine dependent rats is primarily induced by the NMDA receptors activity and the voltage-dependent calcium channels may also be partially involved in the phenomenon.

摘要

利用强直刺激,在吗啡依赖大鼠海马脑片的Schaffer侧支-CA1锥体细胞突触处,研究了NMDA受体和电压依赖性钙通道在长时程增强(LTP)增强中的作用。群体峰电位的幅度作为突触后兴奋性增加的指标进行测量。分别使用d,l-AP5和硝苯地平作为NMDA受体拮抗剂和电压依赖性钙通道阻滞剂。依赖大鼠脑片的顺向群体峰电位幅度的LTP量更高。用含有D,L-AP5(25 microM)或硝苯地平(10 microM)的人工脑脊液灌注对照或依赖大鼠的脑片并给予强直刺激,结果显示,D,L-AP5完全阻断了对照和依赖大鼠脑片的OPS的LTP,而硝苯地平减弱了依赖脑片中OPS的LTP量,对对照脑片无影响。结果表明,吗啡依赖大鼠海马脑片CA1区OPS的LTP增强主要由NMDA受体活性诱导,电压依赖性钙通道也可能部分参与该现象。

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