Re. Lee et al., Association of adhesive macromolecules with terminal sprouts at the neuromuscular junction after botulinum treatment, OTO H N SUR, 120(2), 1999, pp. 255-261
Small quantities of botulinum toxin (BTX) are useful in the treatment of ce
rtain movement disorders, such as laryngeal spasmodic dysphonia, blepharosp
asm, and cervical dystonia, However, the corrective paralytic effects of BT
X are only temporary, in part because of the formation of remodeled neuromu
scular junctions. Here, we questioned whether various factors within and ne
ar the neuromuscular junction could contribute to the remodeling seen after
BTX treatment. BTX was injected subcutaneously in the region of the levato
r auris longus muscle. At 1-week intervals, levator auris longus muscles we
re removed and examined histochemically, As previously described, BTX treat
ment results in a progressive elongation of end plates. The neural cell adh
esion molecule was not associated with the elongated end plates but was ass
ociated with the BTX-induced nerve sprouts after long intervals (3 to 4 wee
ks). Similarly, after BTX, laminin-l (composed of alpha 1, beta 1, and gamm
a 1 chains) reactivity was associated with the nerve sprouts, but not with
the end plates, Laminin beta 2 reactivity at the end plate dispersed somewh
at within 1 week but remained diffusely associated with the elongating end
plates for up to 5 weeks. Together these results suggest that neural cell a
dhesion molecule and laminins may participate in the sprouting observed aft
er BTX treatment and that alterations in laminin beta 2 expression may part
icipate in initial loss of contacts.