Abstract
Previously, we reported that db/db mouse, a leptin receptor null mutant, develops mechanical allodynia at early stage of diabetes from 8 to 12 wk of age. Using this window of pain behaviors, we detected increased phosphorylation of mitogen activated protein kinases (MAPK) in the dorsal root ganglion (DRG) of db/db mice. In the DRG, members of MAPK, including ERK1/2, p38, are phosphorylated prior and during the period of pain behaviors as demonstrated by the immunoblots for the phosphorylated protein.
Highlights
Painful Diabetic Neuropathy (PDN) affects more than 25% of patients with type 2 diabetes; the pathogenesis remains unclear due to lack of knowledge of the molecular mechanisms leading to PDN
We reported that db/db mice develop features of PDN, including mechanical allodynia at 6-12 wk of age and evident sensory neuropathy at 24 wk of age [15,17]
We reported that the mechanical allodynia in db/db mice is concordantly associated increased nerve growth factor (NGF)/Trk A receptor signaling in dorsal root ganglian (DRG) neurons
Summary
Painful Diabetic Neuropathy (PDN) affects more than 25% of patients with type 2 diabetes; the pathogenesis remains unclear due to lack of knowledge of the molecular mechanisms leading to PDN. We have demonstrated that the C57BLK db/db (db/db) mouse, a model of type 2 diabetes that carries the loss-of-function leptin receptor mutant, develops mechanical allodynia in the hind paws during the early stage (6-12 wk of age) of diabetes. Using this timeline of PDN, we can investigate the signaling mechanisms underlying mechanical allodynia in the db/db mouse. Current treatments for PDN are not effective and less than 30% of patients obtain satisfactory pain relief [6]
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