Sawada M, Ichinose M
Department of Physiology, Shimane Medical University, Izumo, Japan.
Neurosci Lett. 1996 Aug 9;213(3):213-5. doi: 10.1016/0304-3940(96)12847-0.
The amyloid beta protein (A beta P) is the major component of the amyloid deposition which characterizes Alzheimer's disease. Effects of extracellularly applied A beta P on the gamma-aminobutyric acid (GABA)-induced Cl- current recorded from identified neurons (R9 and R12) of Aplysia kurodai were investigated with conventional voltage-clamp and pressure ejection techniques. Focal application of 100 nM A beta P (1-40) reduced the GABA-induced hyperpolarization at resting membrane potential and the GABA-induced Cl- current in the neurons held at -50 mV. Bath-applied 100 nM A beta P fragments (1-40) and (25-35) but not A beta P (1-16) inhibited the GABA-induced Cl- current as well as muscimol-induced Cl- currents in the neurons without affecting the resting membrane conductance or holding current. These results suggest that A beta P may increase neuronal excitability by inhibiting GABA-induced Cl- current in the neurons of mammalian central nervous system.
淀粉样β蛋白（AβP）是淀粉样沉积的主要成分，淀粉样沉积是阿尔茨海默病的特征。采用传统电压钳和压力喷射技术，研究了细胞外施加AβP对从日本黑兔确定的神经元（R9和R12）记录的γ-氨基丁酸（GABA）诱导的Cl-电流的影响。局部施加100 nM AβP（1-40）可降低静息膜电位下GABA诱导的超极化以及保持在-50 mV的神经元中GABA诱导的Cl-电流。浴槽施加100 nM AβP片段（1-40）和（25-35），但不是AβP（1-16），可抑制神经元中GABA诱导的Cl-电流以及蝇蕈醇诱导的Cl-电流，而不影响静息膜电导或保持电流。这些结果表明，AβP可能通过抑制哺乳动物中枢神经系统神经元中GABA诱导的Cl-电流来增加神经元兴奋性。
