Journal
JOURNAL OF NEUROSCIENCE
Volume 30, Issue 31, Pages 10360-10368Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1041-10.2010
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Funding
- Academia Sinica [AS95IBMS6]
- National Science Council (NSC), Taiwan [NSC-95-2320-B-001-030, NSC-95 - 2320-B-001-036, NSC-96-2311-B-001-041-MY2]
- NSC of Taiwan [NSC97-3112-B-001-025]
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Treatments for chronic musculoskeletal pain, such as lower back pain, fibromyalgia, and myofascial pain syndrome, remain inadequate because of our poor understanding of the mechanisms that underlie these conditions. Although T-type Ca2+ channels (T-channels) have been implicated in peripheral and central pain sensory pathways, their role in chronic musculoskeletal pain is still unclear. Here, we show that acid-induced chronic mechanical hyperalgesia develops in Ca(v)3.1-deficient and wild-type but not in Ca(v)3.2-deficient male and female mice. We also show that T-channels are required for the initiation, but not maintenance, of acid-induced chronic muscle pain. Blocking T-channels using ethosuximide prevented chronic mechanical hyperalgesia in wild-type mice when administered intraperitoneally or intracerebroventricularly, but not intramuscularly or intrathecally. Furthermore, we found an acid-induced, Ca(v)3.2 T-channel-dependent activation of ERK (extracellular signal-regulated kinase) in the anterior nucleus of paraventricular thalamus (PVA), and prevention of the ERK activation abolished the chronic mechanical hyperalgesia. Our findings suggest that Ca(v)3.2 T-channel-dependent activation of ERK in PVA is required for the development of acid-induced chronic mechanical hyperalgesia.
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