Hösli L, Andrès P F, Hösli E
Neurosci Lett. 1979 Feb;11(2):193-6. doi: 10.1016/0304-3940(79)90126-5.
4-Aminopyridine (4-AP) which selectively blocks K+-conductance of excitable membranes, reversibly abolished the depolarization by gamma-aminobutyric acid (GABA) of cultured satellite glial (SG) cells, but did not or only slightly affect the action of GABA on dorsal root ganglion (DRG) neurons. It is therefore suggested that the depolarization of glial cells by GABA is an indirect effect due to the accumulation of K+ which is released from adjacent neurons during their depolarization by the amino acid. Tetraethylammonium (TEA) had no effect on the GABA depolarization at a concentration of 15 mM but produced a slight reduction at higher concentrations (60--70 mM).
4-氨基吡啶(4-AP)可选择性阻断可兴奋膜的钾离子电导,它能可逆地消除培养的卫星神经胶质(SG)细胞因γ-氨基丁酸(GABA)引起的去极化,但对GABA作用于背根神经节(DRG)神经元没有影响或仅有轻微影响。因此表明,GABA引起的神经胶质细胞去极化是一种间接效应,这是由于在氨基酸使相邻神经元去极化过程中释放的钾离子积累所致。在浓度为15 mM时,四乙铵(TEA)对GABA去极化没有影响,但在较高浓度(60 - 70 mM)时会使其略有降低。