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

Abstract

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 dosedependent decrease in the peak amplitude and acceleration of I_Tau desensitization. Addition of 100 nM β-amyloid peptide (Aβ) to the perfusate caused acceleration of I_Tau desensitization. The effects of Aβ and H⁺ on the rate of I_Tau desensitization were not additive. In addition, Aβ 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, Aβ did not modulate the effects of H⁺ on GABA receptors.