Abstract
Small quantities of botulinum toxin (BTX) are useful in the treatment of certain movement disorders, such as laryngeal spasmodic dysphonia, blepharo-spasm, and cervical dystonia. However, the corrective paralytic effects of BTX are only temporary, in part because of the formation of remodeled neuro-muscular junctions. Here, we questioned whether various factors within and near the neuromuscular junction could contribute to the remodeling seen after BTX treatment. BTX was injected subcutaneously in the region of the levator auris longus muscle. At 1-week intervals, levator auris longus muscles were removed and examined histochemically. As previously described, BTX treatment results in a progressive elongation of end plates. The neural cell adhesion molecule was not associated with the elongated end plates but was associated with the BTX-induced nerve sprouts after long intervals (3 to 4 weeks). Similarly, after BTX, laminin-1 (composed of α1, β1, and γ1 chains) reactivity was associated with the nerve sprouts, but not with the end plates. Laminin β2 reactivity at the end plate dispersed somewhat within 1 week but remained diffusely associated with the elongating end plates for up to 5 weeks. Together these results suggest that neural cell adhesion molecule and laminins may participate in the sprouting observed after BTX treatment and that alterations in laminin β2 expression may participate in initial loss of contacts.
Get full access to this article
View all access options for this article.