抗癫痫药物非氨酯对大鼠海马切片CA1区长期增强作用的影响。

Effects of the antiepileptic drug felbamate on long-term potentiation in the CA1 region of rat hippocampal slices.

作者信息

Pugliese A M, Corradetti R

机构信息

Dipartimento di Farmacologia Preclinica e Clinica Mario Aiazzi-Mancini Università di Firenze, Italy.

出版信息

Neurosci Lett. 1996 Aug 30;215(1):21-4. doi: 10.1016/s0304-3940(96)12948-7.

DOI:10.1016/s0304-3940(96)12948-7

PMID:8880744

Abstract

In the CA1 region of rat hippocampal slices, the antiepileptic drug 2-phenyl-1,3-propanediol dicarbamate (felbamate; 100-1300 microM) concentration-dependently decreased extracellularly recorded synaptic potentials. The effect was significant at 200 microM, and became maximal at 700 microM felbamate, with a 70% decrease in population spike amplitude and 25% reduction of dendritic field excitatory postsynaptic potential (fEPSP) slope. Both alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptor-mediated components of the fEPSP were decreased by 700 microM felbamate. Up to 300 microM felbamate did not affect long-term potentiation (LTP), whereas 500 microM decreased the magnitude of LTP. Higher concentrations of felbamate (700-1300 microM) blocked induction of somatic and dendritic LTP completely, but reversibly. It appears that the concentrations of felbamate which affect LTP are higher than those needed for its antiepileptic action.

摘要

在大鼠海马切片的CA1区，抗癫痫药物2-苯基-1,3-丙二醇二氨基甲酸酯（非氨酯；100 - 1300微摩尔）可浓度依赖性地降低细胞外记录的突触电位。在200微摩尔时该效应显著，在700微摩尔非氨酯时达到最大，群体峰电位幅度降低70%，树突野兴奋性突触后电位（fEPSP）斜率降低25%。700微摩尔非氨酯可使fEPSP中由α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）和N-甲基-D-天冬氨酸（NMDA）受体介导的成分均降低。高达300微摩尔的非氨酯不影响长时程增强（LTP），而500微摩尔可降低LTP的幅度。更高浓度的非氨酯（700 - 1300微摩尔）可完全但可逆地阻断体细胞和树突LTP的诱导。似乎影响LTP的非氨酯浓度高于其抗癫痫作用所需的浓度。