Journal ArticleDOI
Botulinum Toxin Type A Reduces Hyperalgesia and TRPV1 Expression in Rats with Neuropathic Pain
TLDR
Upregulation of TRPV1 expression in the DRG is an important mechanism of neuropathic pain induced by the VRT and the analgesic effect of BTX-A is most likely mediated through reduction of TRpV1expression in the nociceptors.Abstract:
Objective. We aim to determine the effects of botulinum toxin type A (BTX-A) on the thresholds of pain and the expression of transient receptor potential vanilloid type 1 (TRPV1) in the dorsal root ganglion (DRG) in rats with neuropathic pain induced by selective ventral root transection (VRT).
Methods. Neuropathic pain was induced by transection of the lumbar 5 ventral root in male Sprague-Dawley rats. BTX-A or saline was administered to the plantar surface by subcutaneous injection. SB366791 (an inhibitor of TRPV1) was administered intraperitoneally. Behavioral tests were conducted preoperatively and at predefined postoperative days. The expression of TRPV1 was detected and quantified by immunohistochemistry and Western blotting at postoperative days 3, 7, 14, and 21.
Results. TRPV1 expression increased significantly in the L4 ∼5 dorsal root ganglia 7 days after L5 VRT compared with the sham-operated control ( P < 0.05). This increase persisted for at least 21 days. The thresholds of foot withdrawal to mechanical and thermal stimulation decreased significantly as well. Subcutaneous injection of BTX-A significantly and dose-dependently reduced the expression of TRPV1 ( P < 0.05) and partially reversed the pain thresholds.
Conclusion. Upregulation of TRPV1 expression in the DRG is an important mechanism of neuropathic pain induced by the VRT. The analgesic effect of BTX-A is most likely mediated through reduction of TRPV1 expression in the nociceptors.read more
Citations
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Journal ArticleDOI
Calcium-Permeable Ion Channels in Pain Signaling
Emmanuel Bourinet,Christophe Altier,Michael E. Hildebrand,Tuan Trang,Michael W. Salter,Gerald W. Zamponi +5 more
TL;DR: A broad overview of different calcium-permeable ion channels in the afferent pain pathway and their role in pain pathophysiology is provided.
Journal ArticleDOI
Botulinum toxin A, brain and pain.
Ivica Matak,Zdravko Lacković +1 more
TL;DR: It is proposed that the hypothesis of peripheral site of BoNT/A action is not sufficient to explain the experimental data collected up to now and compares the data in favor of peripheral vs. central site and mechanism of action.
Journal ArticleDOI
Mechanisms of Botulinum Toxin Type A Action on Pain.
TL;DR: The effects contributing to these advantageous properties of BoNT/A in pain therapy, specific actions along the nociceptive pathway, consequences of its central activities, the molecular mechanisms of actions in neurons, and general pharmacokinetic parameters are summarized.
Journal ArticleDOI
Therapeutic efficacy and safety of Botulinum Toxin A Therapy in Trigeminal Neuralgia: a systematic review and meta-analysis of randomized controlled trials
Mostafa Ebraheem Morra,Ahmed Elgebaly,Ahmed Elmaraezy,Adham M. Khalil,Ahmed M Altibi,Tran Le Huy Vu,Mostafa Reda Mostafa,Nguyen Tien Huy,Kenji Hirayama +8 more
TL;DR: The results suggest that BTX-A may be an effective and safe treatment option for patients with TN and larger and well-designed RCTs are encouraged to translate these findings into better clinical outcome and better quality of life for TN patients.
Journal ArticleDOI
Botulinum toxin B in the sensory afferent: transmitter release, spinal activation, and pain behavior.
Marc J. Marino,Tetsuji Terashima,Joanne Steinauer,Kelly A. Eddinger,Tony L. Yaksh,Qinghao Xu +5 more
TL;DR: Results indicate that BoNT‐B, after unilateral intraplantar delivery, is taken up by the peripheral terminal, is locally active (blocking plasma extravasation), is transported to the ipsilateral DRG to cleave VAMP, and is acting presynaptically to block release from the spinal peptidergic terminal.
References
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