beta-Amyloid Peptide Antagonizes the Effect of Protons on Taurine-Induced Chloride Current in Rat Hippocampal Pyramidal Neurons

摘要

Taurine is an important endogenous agonist of glycine receptors (GlyR). Using the patchclamp technique, we measured chloride current induced by a short (600 msec) application of taurine (I-Tau) on isolated rat pyramidal neurons. pH of taurine solution in the applicator pipette was neutral (7.4) or acidic (7.0-5.0). Application of protons to a neuron causes a dose-dependent decrease in the peak amplitude and acceleration of I-Tau desensitization. Addition of 100 nM beta-amyloid peptide (A beta) to the perfusate caused acceleration of I-Tau desensitization. The effects of A beta and H+ on the rate of I-Tau desensitization were not additive. In addition, A beta attenuated the effect of H+ on the peak amplitude of I-Tau. We also studied the effect of protons on the chloride current caused by activation of GABA receptors. In contrast to H+ effects on GlyR, A beta did not modulate the effects of H+ on GABA receptors.