Botulinum Neurotoxin Type A Subtype 2 Confers Greater Safety than Subtype 1 in a Rat Parkinson’s Disease Model

Botulinum neurotoxin type A (BoNT/A) cleaves SNAP-25 and interrupts the release of acetylcholine. We previously reported that BoNT/A subtype 2 (BoNT/A2) ameliorates pathologic behavior more effectively than subtype 1 (BoNT/A1) in a rat Parkinson’s disease model. Here, we further show BoNT/A2 has few...

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Detalles Bibliográficos
Autores principales: ITAKURA, Masanori, KOHDA, Tomoko, KUBO, Takeya, SEMI, Yuko, NISHIYAMA, Kazuhiro, AZUMA, Yasu-Taka, NAKAJIMA, Hidemitsu, KOZAKI, Shunji, TAKEUCHI, Tadayoshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Japanese Society of Veterinary Science 2014
Materias:
Pharmacology
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4155206/
https://www.ncbi.nlm.nih.gov/pubmed/24849052
http://dx.doi.org/10.1292/jvms.14-0184
Descripción
Sumario:Botulinum neurotoxin type A (BoNT/A) cleaves SNAP-25 and interrupts the release of acetylcholine. We previously reported that BoNT/A subtype 2 (BoNT/A2) ameliorates pathologic behavior more effectively than subtype 1 (BoNT/A1) in a rat Parkinson’s disease model. Here, we further show BoNT/A2 has fewer adverse effects than BoNT/A1. We first confirmed that intrastriatal treatments of both BoNT/As had no-effect on dopaminergic terminals in the striatum. SNAP-25 cleaved by BoNT/A2 was strictly localized to the striatum on the injected side; however, SNAP-25 cleaved by BoNT/A1 diffused contralaterally. Furthermore, treatment with BoNT/A1 caused a significant reduction in body weight, while BoNT/A2 treatment did not. These results suggest that BoNT/A2 is more beneficial for clinical application against Parkinson’s disease than BoNT/A1.

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