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Title: TRPA1 activation by lidocaine in nerve terminals results in glutamate release increase

Abstract

We examined the effects of local anesthetics lidocaine and procaine on glutamatergic spontaneous excitatory transmission in substantia gelatinosa (SG) neurons in adult rat spinal cord slices with whole-cell patch-clamp techniques. Bath-applied lidocaine (1-5 mM) dose-dependently and reversibly increased the frequency but not the amplitude of spontaneous excitatory postsynaptic current (sEPSC) in SG neurons. Lidocaine activity was unaffected by the Na{sup +}-channel blocker, tetrodotoxin, and the TRPV1 antagonist, capsazepine, but was inhibited by the TRP antagonist, ruthenium red. In the same neuron, the TRPA1 agonist, allyl isothiocyanate, and lidocaine both increased sEPSC frequency. In contrast, procaine did not produce presynaptic enhancement. These results indicate that lidocaine activates TRPA1 in nerve terminals presynaptic to SG neurons to increase the spontaneous release of L-glutamate.

Authors:
; ; ; ; ;  [1];  [1]
  1. Department of Physiology, Saga Medical School, 5-1-1 Nabeshima, Saga 849-8501 (Japan)
Publication Date:
OSTI Identifier:
21255893
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 379; Journal Issue: 4; Other Information: DOI: 10.1016/j.bbrc.2008.12.183; PII: S0006-291X(09)00005-9; Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ADULTS; ISOTHIOCYANATES; NERVE CELLS; PROCAINE; RATS; SODIUM IONS; SPINAL CORD

Citation Formats

Piao, L -H, Fujita, Tsugumi, Jiang, C -Y, Tao, Liu, Yue, H -Y, Nakatsuka, Terumasa, and Kumamoto, Eiichi. TRPA1 activation by lidocaine in nerve terminals results in glutamate release increase. United States: N. p., 2009. Web. doi:10.1016/j.bbrc.2008.12.183.
Piao, L -H, Fujita, Tsugumi, Jiang, C -Y, Tao, Liu, Yue, H -Y, Nakatsuka, Terumasa, & Kumamoto, Eiichi. TRPA1 activation by lidocaine in nerve terminals results in glutamate release increase. United States. https://doi.org/10.1016/j.bbrc.2008.12.183
Piao, L -H, Fujita, Tsugumi, Jiang, C -Y, Tao, Liu, Yue, H -Y, Nakatsuka, Terumasa, and Kumamoto, Eiichi. 2009. "TRPA1 activation by lidocaine in nerve terminals results in glutamate release increase". United States. https://doi.org/10.1016/j.bbrc.2008.12.183.
@article{osti_21255893,
title = {TRPA1 activation by lidocaine in nerve terminals results in glutamate release increase},
author = {Piao, L -H and Fujita, Tsugumi and Jiang, C -Y and Tao, Liu and Yue, H -Y and Nakatsuka, Terumasa and Kumamoto, Eiichi},
abstractNote = {We examined the effects of local anesthetics lidocaine and procaine on glutamatergic spontaneous excitatory transmission in substantia gelatinosa (SG) neurons in adult rat spinal cord slices with whole-cell patch-clamp techniques. Bath-applied lidocaine (1-5 mM) dose-dependently and reversibly increased the frequency but not the amplitude of spontaneous excitatory postsynaptic current (sEPSC) in SG neurons. Lidocaine activity was unaffected by the Na{sup +}-channel blocker, tetrodotoxin, and the TRPV1 antagonist, capsazepine, but was inhibited by the TRP antagonist, ruthenium red. In the same neuron, the TRPA1 agonist, allyl isothiocyanate, and lidocaine both increased sEPSC frequency. In contrast, procaine did not produce presynaptic enhancement. These results indicate that lidocaine activates TRPA1 in nerve terminals presynaptic to SG neurons to increase the spontaneous release of L-glutamate.},
doi = {10.1016/j.bbrc.2008.12.183},
url = {https://www.osti.gov/biblio/21255893}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 4,
volume = 379,
place = {United States},
year = {Fri Feb 20 00:00:00 EST 2009},
month = {Fri Feb 20 00:00:00 EST 2009}
}