scholarly journals Peripherally Administered Botulinum Toxin Type A Localizes Bilaterally in Trigeminal Ganglia of Animal Model

Toxins ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 704
Author(s):  
Arief Waskitho ◽  
Yumiko Yamamoto ◽  
Swarnalakshmi Raman ◽  
Fumiya Kano ◽  
Huijiao Yan ◽  
...  

Peripheral nerve injury leads to sensory ganglion hyperexcitation, which increases neurotransmitter release and neuropathic pain. Botulinum toxin type A (BoNT/A) regulates pain transmission by reducing neurotransmitter release, thereby attenuating neuropathic pain. Despite multiple studies on the use of BoNT/A for managing neuropathic pain in the orofacial region, its exact mechanism of transport remains unclear. In this study, we investigated the effects of BoNT/A in managing neuropathic pain in two different animal models and its transport mechanism in the trigeminal nerve. Intraperitoneal administration of cisplatin induced bilateral neuropathic pain in the orofacial region, reducing the head withdrawal threshold to mechanical stimulation. Unilateral infraorbital nerve constriction (IONC) also reduced the ipsilateral head withdrawal threshold to mechanical stimulation. Unilateral peripheral administration of BoNT/A to the rat whisker pad attenuated cisplatin-induced pain behavior bilaterally. Furthermore, contralateral peripheral administration of BoNT/A attenuated neuropathy-induced behavior caused by IONC. We also noted the presence of BoNT/A in the blood using the mouse bioassay. In addition, the Alexa Fluor-488-labeled C-terminal half of the heavy chain of BoNT/A (BoNT/A-Hc) was localized in the neurons of the bilateral trigeminal ganglia following its unilateral administration. These findings suggest that axonal and hematogenous transport are involved in the therapeutic effects of peripherally administered BoNT/A in the orofacial region.

Author(s):  
Abdelghani Mowafak

The landmark paper discussed in this chapter is ‘Botulinum toxin type A induces direct analgesic effects in chronic neuropathic pain’, published by Ranoux et al. in 2008. The muscle-relaxant properties of botulinum toxin type A (BTX-A) have long been known and used therapeutically. However, BTX-A actions independent of those affecting neuromuscular function had previously only been alluded to, via the observation that BTX-A injections alleviated pain more than would have been expected through the treatment of muscle spasm alone. This paper was one of the first to specifically examine the efficacy of BTX-A in neuropathic pain and was a catalyst for further investigation into BTX-A as a novel analgesic.


2013 ◽  
Vol 29 (11) ◽  
pp. 1006-1012 ◽  
Author(s):  
Gustavo Fabregat ◽  
José De Andrés ◽  
Vicente L. Villanueva-Pérez ◽  
Juan M. Asensio-Samper

2016 ◽  
Vol 79 (4) ◽  
pp. 569-578 ◽  
Author(s):  
Zee‐A Han ◽  
Dae Heon Song ◽  
Hyun‐Mi Oh ◽  
Myung Eun Chung

2021 ◽  
Author(s):  
Huilian Bu ◽  
Huilian Bu ◽  
Pengfei Jiao ◽  
Pengfei Jiao ◽  
Xiaochong Fan ◽  
...  

Abstract Botulinum toxin type A (BTX-A) was widely used to treat neuropathic pain in clinic. The underlying analgesic mechanism of BTX-A involves in axonal transport. The chemokine (C-X-C motif) ligand 13 (CXCL13) and GABA transporter 1 (GAT-1) played important roles in chronic pain. We established a chronic constriction injury (CCI) model. The pain behaviors of rats were measured by testing paw withdrawal thresholds (PWTs) and paw withdrawal latencies (PWLs). The level of proteins was measured by western blots. In our results, the CCI rats showed decrease of PWTs and PWLs, which were relieved by BTX-A. BTX-A reversed the over-expression of CXCL13 and GAT-1 in spinal cord, DRG, sciatic nerve and plantar in CCI rats and characterized in dose-dependent manner. The inhibition of BTX-A on proteins we examined didn’t show significant trend among time points. The analgesic effect of BTX-A disappeared after the axon transport of sciatic nerve blocked by the colchicine. But the PWTs of the colchicine treated CCI rats were higher than non- colchicine-treated CCI rats. Colchicine decreased the levels of CXCL13 and GAT-1 in CCI rats. What’s more, the proteins we examined peaked at the sciatic nerve in the non-colchicine group, but the phenomenon disappeared in the colchicine group. In conclusion, the BTX-A and colchicine relieve neuropathic pain and suppress the increase of CXCL13 and GAT-1. Colchicine prevents the analgesic effect of BTX-A by blocking axon transport. The axon transport may play roles in the peripheral mechanisms of neuropathic pain.


2019 ◽  
Vol 77 (5) ◽  
pp. 346-351 ◽  
Author(s):  
Emanuel de Jesus Soares de Sousa ◽  
Gustavo Celeira de Sousa ◽  
Vitor Ferreira Baia ◽  
Danusa Neves Somensi ◽  
Marília Brasil Xavier

ABSTRACT Neuropathic pain is a chronic syndrome that is difficult to treat and often affects patients with leprosy. Recommended treatment includes the the use of analgesic drugs, codeine, tricyclic antidepressants, neuroleptics, anticonvulsants and thalidomide, but without consensus on uniform dose and fully satisfactory results. Objective: To analyze botulinum toxin type A (BoNT-A) effectiveness in treatment of chronic neuropathic pain in refractory leprous patients, as well as evaluate and compare the quality of life of patients before and after using the medication. Methods: We used a specific protocol including clinical, demographic, DN4 protocol, analogue scale (VAS), sensory evaluation and evaluation of the WHOQOL-BREF. Therapeutic intervention was performed with BOTOX® BTX-A 100U administered subcutaneously. Fifteen patients were evaluated on days 0, 10 and 60. Results: Patients on VAS showed pain between 5 and 10, in one case there was complete pain relief in 60 days, while others showed improvement in the first week with the return of symptoms with less intensity after this period. WHOQOL-BREF's domains Quality of Life and Physical to have a significant increase in QOL. Conclusion: BoNT-A proved to be a good therapeutic option in relieving pain with improved quality of life for these patients.


Sign in / Sign up

Export Citation Format

Share Document