Acrylamide inhibits nerve sprouting induced by botulinum toxin type A

Abstract

Botulinum toxin type A is a potent muscle relaxant that blocks the transmission and release of acetylcholine at the neuromuscular junction. Intramuscular injection of botulinum toxin type A has served as an effective and safe therapy for strabismus and focal dystonia. However, muscular weakness is temporary and after 3–4 months, muscle strength usually recovers because functional recovery is mediated by nerve sprouting and reconstruction of the neuromuscular junction. Acrylamide may produce neurotoxic substances that cause retrograde necrotizing neuropathy and inhibit nerve sprouting caused by botulinum toxin type A. This study investigated whether acrylamide inhibits nerve sprouting after intramuscular injection of botulinum toxin type A. A tibial nerve sprouting model was established through local injection of botulinum toxin type A into the right gastrocnemius muscle of Sprague-Dawley rats. Following intramuscular injection, rats were given intraperitoneal injection of 3% acrylamide every 3 days for 21 days. Nerve sprouting appeared 2 weeks after intramuscular injection of botulinum toxin type A and single-fiber electromyography revealed abnormal conduction at the neuromuscular junction 1 week after intramuscular injection of botulinum toxin type A. Following intraperitoneal injection of acrylamide, the peak muscle fiber density decreased. Electromyography jitter value were restored to normal levels 6 weeks after injection. This indicates that the maximal decrease in fiber density and the time at which functional conduction of neuromuscular junction was restored were delayed. Additionally, the increase in tibial nerve fibers was reduced. Acrylamide inhibits nerve sprouting caused by botulinum toxin type A and may be used to prolong the clinical dosage of botulinum toxin type A.

Contribution of Single-Fiber Evaluation on Monitoring Outcomes Following Injection of Botulinum Toxin-A: A Narrative Review of the Literature

“…Five systematic or narrative reviews on the clinical spectrum of botulism [ 75 ], clinical impact of SFEMG [ 76 , 77 ] and botulinum toxin in neurological disease [ 78 , 79 ] were excluded after reading and selecting references of interest (20 references). Finally, four animal studies were excluded [ 80 , 81 , 82 , 83 ].…”

Botulinum Toxin Induced Atrophy: An Uncharted Territory

“…Sprouting is the process by which the functional recovery of neuromuscular transmission occurs following chemodenervation by BoNTs. Interruption of sprouting could leave the muscles “functionally denervated” leading to atrophy [ 42 , 43 , 44 , 45 ]. Several elements influence sprouting, such as Insulin like Growth Factor (IGF)-1, Schwann cells, motor axon length and fiber type composition.…”