Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
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Target Concepts:
Gene/Protein
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Query: UMLS:C0151825 (
bone pain
)
3,118
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Nav1.7
, a peripheral neuron voltage-gated sodium channel, is essential for pain and olfaction in mice and humans. We examined the role of
Nav1.7
as well as Nav1.3, Nav1.8, and Nav1.9 in different mouse models of chronic pain. Constriction-injury-dependent neuropathic pain is abolished when
Nav1.7
is deleted in sensory neurons, unlike nerve-transection-related pain, which requires the deletion of
Nav1.7
in sensory and sympathetic neurons for pain relief. Sympathetic sprouting that develops in parallel with nerve-transection pain depends on the presence of
Nav1.7
in sympathetic neurons. Mechanical and cold allodynia required distinct sets of neurons and different repertoires of sodium channels depending on the nerve injury model. Surprisingly, pain induced by the chemotherapeutic agent oxaliplatin and cancer-induced
bone pain
do not require the presence of
Nav1.7
sodium channels or Nav1.8-positive nociceptors. Thus, similar pain phenotypes arise through distinct cellular and molecular mechanisms. Therefore, rational analgesic drug therapy requires patient stratification in terms of mechanisms and not just phenotype.
...
PMID:Pain without nociceptors? Nav1.7-independent pain mechanisms. 2448 69
