Anoctamin-1 Cl− Channels in Nociception: Activation by an N-Aroylaminothiazole and Capsaicin and Inhibition by T16A[inh]-A01-Reference-Cited by-同舟云学术

Anoctamin-1 Cl− Channels in Nociception: Activation by an N-Aroylaminothiazole and Capsaicin and Inhibition by T16A[inh]-A01

Published:2015-08-28 Issue: Volume:11 Page:s12990-015-0061
ISSN:1744-8069
Container-title:Molecular Pain
language:en
Short-container-title:Mol Pain

Author:

Deba Farah¹,Bessac Bret F.¹

Affiliation:

1. Department of Pharmaceutical Sciences, I. L. Rangel College of Pharmacy, Texas A&M Health Science Center, 1010 West Avenue B MSC 131, Kingsville, TX 78363, USA

Publisher

SAGE Publications

Subject

Anesthesiology and Pain Medicine,Cellular and Molecular Neuroscience,Molecular Medicine

Link

http://journals.sagepub.com/doi/pdf/10.1186/s12990-015-0061-y

Reference54 articles.

1. Education IoMUSCoAPRCa. Relieving pain in America: a blueprint for transforming prevention, care, education, and research. Washington D.C.: National Academies Press; 2011. p. 364.

2. Peripheral and central mechanisms of cutaneous hyperalgesia

3. The acute nociceptive signals induced by bradykinin in rat sensory neurons are mediated by inhibition of M-type K+ channels and activation of Ca2+-activated Cl– channels

4. Activation of the Cl − Channel ANO1 by Localized Calcium Signals in Nociceptive Sensory Neurons Requires Coupling with the IP 3 Receptor

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