TY - JOUR
T1 - Organization and reorganization of neuromuscular junctions in mice lacking neural cell adhesion molecule, tenascin-C, or fibroblast growth factor-5
AU - Moscoso, Lisa M.
AU - Cremer, Harold
AU - Sanes, Joshua R.
PY - 1998/2/15
Y1 - 1998/2/15
N2 - Many proteins have been hypothesized to mediate intercellular interactions that regulate the formation, maturation, and maintenance of the skeletal neuromuscular junction. Three of the best characterized of these are a membrane-associated adhesion molecule, neural cell adhesion molecule (N- CAM), an extracellular matrix component, tenascin-C, and a soluble growth factor, fibroblast growth factor-5 (FGF-5). To assess the roles of these molecules in synaptogenesis in vivo, we examined neuromuscular junctions in homozygous mutant mice lacking N-CAM, tenascin-C, FGF-5, or both N-CAM and tenascin-C. End plates were 14% smaller in N-CAM-deficient mice than in controls, and formation of junctional folds was delayed in this mutant. In all other respects tested, however, the structure and molecular architecture of neuromuscular junctions were normal in all three single mutants and in the double mutant. We also tested the abilities of damaged motor axons to reinnervate mutant muscle after axotomy and of intact motor axons to sprout after partial denervation. Again, no significant differences among genotypes were observed. Together, these results demonstrate that N-CAM, tenascin-C, and FGF-5 are dispensable for major aspects of synaptic development and regeneration.
AB - Many proteins have been hypothesized to mediate intercellular interactions that regulate the formation, maturation, and maintenance of the skeletal neuromuscular junction. Three of the best characterized of these are a membrane-associated adhesion molecule, neural cell adhesion molecule (N- CAM), an extracellular matrix component, tenascin-C, and a soluble growth factor, fibroblast growth factor-5 (FGF-5). To assess the roles of these molecules in synaptogenesis in vivo, we examined neuromuscular junctions in homozygous mutant mice lacking N-CAM, tenascin-C, FGF-5, or both N-CAM and tenascin-C. End plates were 14% smaller in N-CAM-deficient mice than in controls, and formation of junctional folds was delayed in this mutant. In all other respects tested, however, the structure and molecular architecture of neuromuscular junctions were normal in all three single mutants and in the double mutant. We also tested the abilities of damaged motor axons to reinnervate mutant muscle after axotomy and of intact motor axons to sprout after partial denervation. Again, no significant differences among genotypes were observed. Together, these results demonstrate that N-CAM, tenascin-C, and FGF-5 are dispensable for major aspects of synaptic development and regeneration.
KW - FGF
KW - N-CAM
KW - Neuromuscular junction
KW - Reinnervation
KW - Sprouting
KW - Synapse formation
KW - Tenascin
UR - http://www.scopus.com/inward/record.url?scp=0032519649&partnerID=8YFLogxK
U2 - 10.1523/jneurosci.18-04-01465.1998
DO - 10.1523/jneurosci.18-04-01465.1998
M3 - Article
C2 - 9454855
AN - SCOPUS:0032519649
SN - 0270-6474
VL - 18
SP - 1465
EP - 1477
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 4
ER -