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Transient Receptor Potential Channels in Microglia: Roles in Physiology and Disease

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Abstract

Microglia modulate the nervous system cellular environment and induce neuroprotective and neurotoxic effects. Various molecules are involved in these processes, including families of ion channels expressed in microglial cells, such as transient receptor potential (TRP) channels. TRP channels comprise a family of non-selective cation channels that can be activated by mechanical, thermal, and chemical stimuli, and which contribute to the regulation of intracellular calcium concentrations. TRP channels have been shown to be involved in cellular processes such as osmotic regulation, cytokine production, proliferation, activation, cell death, and oxidative stress responses. Given the significance of these processes in microglial activity, studies of TRP channels in microglia have focused on determining their roles in both neuroprotective and neurotoxic processes. TRP channel activity has been proposed to play an important function in neurodegenerative diseases, ischemia, inflammatory responses, and neuropathic pain. Modulation of TRP channel activity may thus be considered as a potential therapeutic strategy for the treatment of various diseases associated with alterations of the central nervous system (CNS). In this review, we describe the expression of different subfamilies of TRP channels in microglia, focusing on their physiological and pathophysiological roles, and consider their potential use as therapeutic targets in CNS diseases.

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Acknowledgments

This work was funded by Pontificia Universidad Javeriana, Grant ID 3699 (Evaluación del efecto de extractos de plantas nativas de uso tradicional para el tratamiento del dolor sobre los canales iónicos TRPV1 y TRPM8) and ID 6587 (Semillero de Investigación en Biofísica y Fisiología de Canales Iónicos) to Torres YP.

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Correspondence to Yolima P. Torres.

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Echeverry, S., Rodriguez, M.J. & Torres, Y.P. Transient Receptor Potential Channels in Microglia: Roles in Physiology and Disease. Neurotox Res 30, 467–478 (2016). https://doi.org/10.1007/s12640-016-9632-6

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  • DOI: https://doi.org/10.1007/s12640-016-9632-6

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