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M2受体参与卡巴胆碱增强海马脑片Schaffer侧支-CA1突触的长时程增强作用。

Involvement of M2 receptor in an enhancement of long-term potentiation by carbachol in Schaffer collateral-CA1 synapses of hippocampal slices.

作者信息

Shimoshige Y, Maeda T, Kaneko S, Akaike A, Satoh M

机构信息

Department of Molecular Pharmacology, Faculty of Pharmaceutical Sciences, Kyoto University, Japan.

出版信息

Neurosci Res. 1997 Feb;27(2):175-80. doi: 10.1016/s0168-0102(96)01147-9.

Abstract

We examined effects of carbachol (CCh), muscarinic receptor agonist, on long-term potentiation (LTP) of field excitatory postsynaptic potential (fEPSP) at Schaffer collateral-CA1 synapse of guinea pig hippocampal slices using extracellular recording technique. Application of 0.1 microM CCh to the slices significantly augmented the magnitude of LTP without significant change in the amplitude of pretetanus fEPSP. The enhancement of LTP by 0.1 microM CCh was significantly attenuated by 0.1 microM AF-DX 116, M2 receptor antagonist, but not by 0.1 microM pirenzepine, M1 receptor antagonist. Ten micromolar of carbachol reduced the amplitude of pretetanus fEPSP, while the magnitude of LTP was significantly larger than that in control slices to which tetanus was applied in a stimulus intensity producing pretetanus fEPSPs with an amplitude comparable to those during administration of 10 microM CCh. Neither 0.1 microM pirenzepine nor 0.1 microM AF-DX 116 had significant effect on the enhancement of LTP by 10 microM CCh. These results suggest that the induction of LTP at Schaffer collateral-CA1 synapse was enhanced through the activation of M2 receptors by CCh at a lower concentration.

摘要

我们采用细胞外记录技术,研究了毒蕈碱受体激动剂卡巴胆碱(CCh)对豚鼠海马脑片Schaffer侧支-CA1突触处场兴奋性突触后电位(fEPSP)的长时程增强(LTP)的影响。向脑片施加0.1微摩尔/升的CCh可显著增强LTP的幅度,而强直刺激前fEPSP的幅度无明显变化。0.1微摩尔/升的M2受体拮抗剂AF-DX 116可显著减弱0.1微摩尔/升CCh对LTP的增强作用,但0.1微摩尔/升的M1受体拮抗剂哌仑西平则无此作用。10微摩尔/升的卡巴胆碱可降低强直刺激前fEPSP的幅度,而LTP的幅度显著大于对照组脑片(对照组脑片施加的强直刺激强度所产生的强直刺激前fEPSP幅度与10微摩尔/升CCh给药期间的幅度相当)。0.1微摩尔/升的哌仑西平或0.1微摩尔/升的AF-DX 116对10微摩尔/升CCh增强LTP均无显著影响。这些结果表明,较低浓度的CCh通过激活M2受体增强了Schaffer侧支-CA1突触处LTP的诱导。

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