Peripheral Leptin Signaling Mediates Formalin-Induced Nociception / 神经科学通报·英文版
Neuroscience Bulletin
;
(6): 321-329, 2018.
Article
in English
| WPRIM
| ID: wpr-777054
ABSTRACT
Accumulating evidence suggests that obesity is associated with chronic pain. However, whether obesity is associated with acute inflammatory pain is unknown. Using a well-established obese mouse model induced by a high-fat diet, we found that (1) the acute thermal pain sensory threshold did not change in obese mice; (2) the model obese mice had fewer nociceptive responses in formalin-induced inflammatory pain tests; restoring the obese mice to a chow diet for three weeks partly recovered their pain sensation; (3) leptin injection induced significant phosphorylation of STAT3 in control mice but not in obese mice, indicating the dysmodulation of topical leptin-leptin receptor signaling in these mice; and (4) leptin-leptin receptor signaling-deficient mice (ob/ob and db/db) or leptin-leptin receptor pathway blockade with a leptin receptor antagonist and the JAK2 inhibitor AG 490 in wild-type mice reduced their nociceptive responses in formalin tests. These results indicate that leptin plays a role in nociception induced by acute inflammation and that interference in the leptin-leptin receptor pathway could be a peripheral target against acute inflammatory pain.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pharmacology
/
Physiology
/
Pain Measurement
/
Signal Transduction
/
Pain Threshold
/
Leptin
/
Receptors, Leptin
/
Nociceptive Pain
/
Nociception
/
Diet, High-Fat
Limits:
Animals
Language:
English
Journal:
Neuroscience Bulletin
Year:
2018
Type:
Article
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