Open AccessA KCa3.1 Channel Opener, ASP0819, Modulates Nociceptive Signal Processing from Peripheral Nerves in Fibromyalgia-Like Pain in Rats
Author(s) -
Nobuaki Takeshita,
Tomoya Oe,
Tetsuo Kiso,
Shuichiro Kakimoto
Publication year - 2021
Publication title -
journal of pain research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.888
H-Index - 49
ISSN - 1178-7090
DOI - 10.2147/jpr.s274563
Subject(s) - medicine , myalgia , peripheral , electrophysiology , fibromyalgia , in vivo , nociception , stimulation , pathophysiology , pharmacology , anesthesia , receptor , biology , microbiology and biotechnology
Although abnormal peripheral and central pain processing has been observed in fibromyalgia (FM) patients, the biomechanics and pathophysiology, surrounding the peripheral mechanism are not well understood. An intermediate conductance channel, K Ca 3.1, is expressed in peripheral sensory nerve fibers where it maintains the resting membrane potential and controls nerve firing, making it a plausible target for peripheral therapeutic interventions. ASP0819, a K Ca 3.1 channel opener, is an orally available molecular entity and is used in this investigation to elucidate the role of K Ca 3.1 in signal processing of pain in FM.