The NA_v1.7 blocker protoxin II reduces burn injury-induced spinal nociceptive processing.

ABSTRACT: Controlling pain in burn-injured patients poses a major clinical challenge. Recent findings suggest that reducing the activity of the voltage-gated sodium channel Na_v1.7 in primary sensory neurons could provide improved pain control in burn-injured patients. Here, we report that partial thickness scalding-type burn injury on the rat paw upregulates Na_v1.7 expression in primary sensory neurons 3 h following injury. The injury also induces upregulation in phosphorylated cyclic adenosine monophosphate response element-binding protein (p-CREB), a marker for nociceptive activation in primary sensory neurons. The upregulation in p-CREB occurs mainly in Na_v1.7-immunopositive neurons and exhibits a peak at 5 min and, following a decline at 30 min, a gradual increas

SUBMITTER: Torres-Perez JV 

PROVIDER: S-EPMC5750333 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature