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 (ITau) 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 ITau desensitization. Addition of 100 nM β-amyloid peptide (Aβ) to the perfusate caused acceleration of ITau desensitization. The effects of Aβ and H+ on the rate of ITau desensitization were not additive. In addition, Aβ attenuated the effect of H+ on the peak amplitude of ITau. 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.
Published Version
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