β-Amyloid Peptide Antagonizes the Effect of Protons on Taurine-Induced Chloride Current in Rat Hippocampal Pyramidal Neurons
- Authors: Solntseva E.I.1, Bukanova Y.V.1, Kondratenko R.V.1, Skrebitsky V.G.1
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Affiliations:
- Research Center of Neurology, Russian Academy of Medical Sciences
- Issue: Vol 167, No 2 (2019)
- Pages: 237-241
- Section: Biophysics and Biochemistry
- URL: https://journals.rcsi.science/0007-4888/article/view/241611
- DOI: https://doi.org/10.1007/s10517-019-04499-9
- ID: 241611
Cite item
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.
About the authors
E. I. Solntseva
Research Center of Neurology, Russian Academy of Medical Sciences
Author for correspondence.
Email: synaptology@mail.ru
Russian Federation, Moscow
Yu. V. Bukanova
Research Center of Neurology, Russian Academy of Medical Sciences
Email: synaptology@mail.ru
Russian Federation, Moscow
R. V. Kondratenko
Research Center of Neurology, Russian Academy of Medical Sciences
Email: synaptology@mail.ru
Russian Federation, Moscow
V. G. Skrebitsky
Research Center of Neurology, Russian Academy of Medical Sciences
Email: synaptology@mail.ru
Russian Federation, Moscow