Primary afferent C-fibers have been regarded as a critical element for the inflammatory reaction and neurokinins stored in the vesicles at the peripheral endings of C-fibers as important inflammatory mediators. Upon excitation of the C-fibers, neurokinins are released from containing vesicles into surrounding tissues, resulting in vasodilatation. Botulinum neurotoxin is known to paralyze muscles by preventing the release of acetylcholine from the vesicles at the peripheral endings of motoneurons. The control mechanisms for vesicular release appear to be extremely similar among almost all eukaryotic organisms, from yeasts, a lower level unicellular organism, to brain cells of advanced primates. Therefore, this study aimed to test the inhibitory effect of botulinum neurotoxin on inflammation and to compare the inhibitory effects with those of lidocaine (a topical anesthetic) and L-733060 (an antagonist for the neurokinin NK-1 type receptor). The results showed that a pre-injection of 5U BOTOX, 2% lidocaine, or L-733060 (1mg/kg) all effectively reduced the evoked inflammation and the botulinum neurotoxin commenced to act 7 days after the pre-injection with a duration of at least 10 days. This study suggests that botulinum neurotoxin has an inhibitory effect on neurogenic inflammation.
|Original language||Traditional Chinese|
|Number of pages||9|
|Publication status||Published - 2005|
- botulinum neurotoxin
- mustard oil
- neurogenic inflammation
- Evans blue extavasation