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Possible involvement of transient receptor potential ankyrin 1 in Ca2+ signaling via T-type Ca2+ channel in mouse sensory neurons.
J Neurosci Res. 2018 05; 96(5):901-910.JN

Abstract

T-type Ca2+ channels and TRPA1 are expressed in sensory neurons and both are associated with pain transmission, but their functional interaction is unclear. Here we demonstrate that pharmacological evidence of the functional relation between T-type Ca2+ channels and TRPA1 in mouse sensory neurons. Low concentration of KCl at 15 mM (15K) evoked increases of intracellular Ca2+ concentration ([Ca2+ ]i), which were suppressed by selective T-type Ca2+ channel blockers. RT-PCR showed that mouse sensory neurons expressed all subtypes of T-type Ca2+ channel. The magnitude of 15K-induced [Ca2+ ]i increase was significantly larger in neurons sensitive to allylisothiocyanate (AITC, a TRPA1 agonist) than in those insensitive to it, and in TRPA1-/- mouse sensory neurons. TRPA1 blockers diminished the [Ca2+ ]i responses to 15K in neurons sensitive to AITC, but failed to inhibit 40 mM KCl-induced [Ca2+ ]i increases even in AITC-sensitive neurons. TRPV1 blockers did not inhibit the 15K-induced [Ca2+ ]i increase regardless of the sensitivity to capsaicin. [Ca2+ ]i responses to TRPA1 agonist were enhanced by co-application with 15K. These pharmacological data suggest the possibility of functional interaction between T-type Ca2+ channels and TRPA1 in sensory neurons. Since TRPA1 channel is activated by intracellular Ca2+ , we hypothesize that Ca2+ entered via T-type Ca2+ channel activation may further stimulate TRPA1, resulting in an enhancement of nociceptive signaling. Thus, T-type Ca2+ channel may be a potential target for TRPA1-related pain.

Authors+Show Affiliations

Department of Veterinary Pharmacology, Faculty of Agriculture, Tottori University, Tottori, Japan.Department of Veterinary Pharmacology, Faculty of Agriculture, Tottori University, Tottori, Japan.Department of Veterinary Pharmacology, Faculty of Agriculture, Tottori University, Tottori, Japan.Division of Cell Signaling, Okazaki Institute for Integrative Bioscience (National Institute for Physiological Sciences), National Institutes of Natural Sciences, Okazaki, Japan.Department of Veterinary Pharmacology, Faculty of Agriculture, Tottori University, Tottori, Japan.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

29282753

Citation

Nishizawa, Yuki, et al. "Possible Involvement of Transient Receptor Potential Ankyrin 1 in Ca2+ Signaling Via T-type Ca2+ Channel in Mouse Sensory Neurons." Journal of Neuroscience Research, vol. 96, no. 5, 2018, pp. 901-910.
Nishizawa Y, Takahashi K, Oguma N, et al. Possible involvement of transient receptor potential ankyrin 1 in Ca2+ signaling via T-type Ca2+ channel in mouse sensory neurons. J Neurosci Res. 2018;96(5):901-910.
Nishizawa, Y., Takahashi, K., Oguma, N., Tominaga, M., & Ohta, T. (2018). Possible involvement of transient receptor potential ankyrin 1 in Ca2+ signaling via T-type Ca2+ channel in mouse sensory neurons. Journal of Neuroscience Research, 96(5), 901-910. https://doi.org/10.1002/jnr.24208
Nishizawa Y, et al. Possible Involvement of Transient Receptor Potential Ankyrin 1 in Ca2+ Signaling Via T-type Ca2+ Channel in Mouse Sensory Neurons. J Neurosci Res. 2018;96(5):901-910. PubMed PMID: 29282753.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Possible involvement of transient receptor potential ankyrin 1 in Ca2+ signaling via T-type Ca2+ channel in mouse sensory neurons. AU - Nishizawa,Yuki, AU - Takahashi,Kenji, AU - Oguma,Naoko, AU - Tominaga,Makoto, AU - Ohta,Toshio, Y1 - 2017/12/28/ PY - 2017/06/05/received PY - 2017/11/06/revised PY - 2017/11/27/accepted PY - 2017/12/29/pubmed PY - 2019/12/24/medline PY - 2017/12/29/entrez KW - intracellular Ca2+ increase KW - low-voltage activated Ca2+ channel KW - sensory neuron SP - 901 EP - 910 JF - Journal of neuroscience research JO - J Neurosci Res VL - 96 IS - 5 N2 - T-type Ca2+ channels and TRPA1 are expressed in sensory neurons and both are associated with pain transmission, but their functional interaction is unclear. Here we demonstrate that pharmacological evidence of the functional relation between T-type Ca2+ channels and TRPA1 in mouse sensory neurons. Low concentration of KCl at 15 mM (15K) evoked increases of intracellular Ca2+ concentration ([Ca2+ ]i), which were suppressed by selective T-type Ca2+ channel blockers. RT-PCR showed that mouse sensory neurons expressed all subtypes of T-type Ca2+ channel. The magnitude of 15K-induced [Ca2+ ]i increase was significantly larger in neurons sensitive to allylisothiocyanate (AITC, a TRPA1 agonist) than in those insensitive to it, and in TRPA1-/- mouse sensory neurons. TRPA1 blockers diminished the [Ca2+ ]i responses to 15K in neurons sensitive to AITC, but failed to inhibit 40 mM KCl-induced [Ca2+ ]i increases even in AITC-sensitive neurons. TRPV1 blockers did not inhibit the 15K-induced [Ca2+ ]i increase regardless of the sensitivity to capsaicin. [Ca2+ ]i responses to TRPA1 agonist were enhanced by co-application with 15K. These pharmacological data suggest the possibility of functional interaction between T-type Ca2+ channels and TRPA1 in sensory neurons. Since TRPA1 channel is activated by intracellular Ca2+ , we hypothesize that Ca2+ entered via T-type Ca2+ channel activation may further stimulate TRPA1, resulting in an enhancement of nociceptive signaling. Thus, T-type Ca2+ channel may be a potential target for TRPA1-related pain. SN - 1097-4547 UR - https://www.unboundmedicine.com/medline/citation/29282753/Possible_involvement_of_transient_receptor_potential_ankyrin_1_in_Ca2+_signaling_via_T_type_Ca2+_channel_in_mouse_sensory_neurons_ L2 - https://doi.org/10.1002/jnr.24208 DB - PRIME DP - Unbound Medicine ER -