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• W2024951037 abstract "Previous studies have indicated that mu-opioid receptors in the thalamic nucleus submedius (Sm) are involved in descending antinociception in behavioral tests. The present study examined the effect of mu-opioid receptor activation in the Sm upon bee venom-evoked c-Fos expression in the spinal dorsal horn associated with flinching behavior, and determined whether the ATP-sensitive potassium channel (K-ATP channel) was involved in this effect in a rat model. A dilute bee venom solution, subcutaneously injected unilaterally into a rat hind paw pad, induced significant c-Fos expression in the lumbar spinal dorsal horn, which is associated with paw flinching behavior. This effect was depressed by microinjection of the mu-opioid receptor agonist [d-Ala2, N-MePhe4, Gly-ol5]-enkephalin (DAMGO) into the Sm, which was antagonized by pre-treatment with mu-receptor antagonist beta-funaltrexamine at the same Sm site. Further studies found that glibenclamide, a K-ATP channel inhibitor, also blocked DAMGO-induced inhibition. These results provide functional anatomic support for the involvement of Sm and mu-opioid receptors in the modulation of persistent inflammatory nociception, and suggest that these effects were produced by opening K-ATP channel and inhibiting neuronal activity. Together with previous studies, the inhibition of the neuronal activity induced by mu-opioid receptor activation may activate descending antinociceptive pathways through a GABAergic disinhibitory mechanism and depress the nociceptive information transmission at the level of the spinal cord." @default.
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• W2024951037 date "2009-06-01" @default.
• W2024951037 modified "2023-09-27" @default.
• W2024951037 title "Activation of mu-opioid receptors in thalamic nucleus submedius depresses bee venom–evoked spinal c-Fos expression and flinching behavior" @default.
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• W2024951037 doi "https://doi.org/10.1016/j.neuroscience.2009.03.066" @default.
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