Hyperinnervation of Neuromuscular Junctions Caused by GDNF Overexpression in Muscle
- 13 March 1998
- journal article
- other
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 279 (5357) , 1725-1729
- https://doi.org/10.1126/science.279.5357.1725
Abstract
Overexpression of glial cell line–derived neurotrophic factor (GDNF) by muscle greatly increased the number of motor axons innervating neuromuscular junctions in neonatal mice. The extent of hyperinnervation correlated with the amount of GDNF expressed in four transgenic lines. Overexpression of GDNF by glia and overexpression of neurotrophin-3 and neurotrophin-4 in muscle did not cause hyperinnervation. Thus, increased amounts of GDNF in postsynaptic target cells can regulate the number of innervating axons.Keywords
This publication has 34 references indexed in Scilit:
- Regulation of spinal motoneuron survival by GDNF during development and following injuryCell and tissue research, 1996
- Neurotrophic Survival Molecules for Motoneurons: An Embarrassment of RichesNeuron, 1996
- Are Neurotrophins Synaptotrophins?Molecular and Cellular Neuroscience, 1996
- Mechanism of synapse disassembly at the developing neuromuscular junctionCurrent Opinion in Neurobiology, 1996
- Ciliary Neurotrophic Factor May Act in Target Musculature to Regulate Developmental Synapse EliminationDevelopmental Neuroscience, 1996
- Effects of brain-derived neurotrophic factor on optic axon branching and remodelling in vivoNature, 1995
- Leukemia inhibitory factor influences the timing of programmed synapse withdrawal from neonatal musclesJournal of Neurobiology, 1995
- Influences of neurotrophins on mammalian motoneurons in vivoJournal of Neurobiology, 1993
- Antimyoclonic Effect of MK-801Clinical Neuropharmacology, 1990
- Postnatal loss of synaptic terminals in the normal mouse soleus muscleActa Physiologica Scandinavica, 1987