Nimodipine suppresses preferential reinnervation of mouse soleus muscles by slow alpha-motoneurons

Citation
Dl. Bishop et Rl. Milton, Nimodipine suppresses preferential reinnervation of mouse soleus muscles by slow alpha-motoneurons, EXP NEUROL, 154(2), 1998, pp. 366-370
Citations number
43
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EXPERIMENTAL NEUROLOGY
ISSN journal
00144886 → ACNP
Volume
154
Issue
2
Year of publication
1998
Pages
366 - 370
Database
ISI
SICI code
0014-4886(199812)154:2<366:NSPROM>2.0.ZU;2-9
Abstract
Denervation of mouse soleus muscle followed by self-reinnervation causes a significant increase in slow twitch (type I) muscle fiber content, suggesti ng preferential reinnervation by slow alpha-motoneurons. Since intracellula r Ca2+ influences both axonal elongation rate and branching, we examined th e process of self-reinnervation in mouse soleus muscles in the presence of the L-type Ca2+ channel blocker nimodipine. Soleus muscles in both control and experimental animals were denervated by crushing the soleus nerve where it enters the muscle. Experimental animals received a daily i.p. injection of a 0.1% nimodipine solution beginning 4 days prior to denervation and en ding 2 weeks postdenervation. At 2 months postdenervation reinnervated and contralateral muscles from both control and experimental animals were secti oned and histochemically stained for myosin ATPase to determine the percent age of slow twitch fibers in the muscles. It was found that, in agreement w ith previous experiments, untreated reinnervated muscles had a significantl y higher percentage of slow twitch fibers than did their contralateral cont rols (91.3 versus 74.6%). However, in nimodipine-treated animals only a sma ll, but not statistically significant, difference between reinnervated and contralateral control muscles was observed (76.5 versus 72.8%). These resul ts suggest that Ca2+ influx through L-type calcium channels in growing neur ites may play a role in the outcome of the reinnervation process. (C) 1998 Academic Press.