GONUTS has been updated to MW1.31 Most things seem to be working but be sure to report problems.
TableEdit
PMID:12533614
You don't have sufficient rights on this wiki to edit tables. Perhaps you need to log in. Changes you make in the Table editor will not be saved back to the wiki
See Help for Help on this wiki. See the documentation for how to use the table editor
Citation |
Brandon, EP, Lin, W, D'Amour, KA, Pizzo, DP, Dominguez, B, Sugiura, Y, Thode, S, Ko, CP, Thal, LJ, Gage, FH and Lee, KF (2003) Aberrant patterning of neuromuscular synapses in choline acetyltransferase-deficient mice. J. Neurosci. 23:539-49 |
---|---|
Abstract |
In this study we examined the developmental roles of acetylcholine (ACh) by establishing and analyzing mice lacking choline acetyltransferase (ChAT), the biosynthetic enzyme for ACh. As predicted, ChAT-deficient embryos lack both spontaneous and nerve-evoked postsynaptic potentials in muscle and die at birth. In mutant embryos, abnormally increased nerve branching occurs on contact with muscle, and hyperinnervation continues throughout subsequent prenatal development. Postsynaptically, ACh receptor clusters are markedly increased in number and occupy a broader muscle territory in the mutants. Concomitantly, the mutants have significantly more motor neurons than normal. At an ultrastructural level, nerve terminals are smaller in mutant neuromuscular junctions, and they make fewer synaptic contacts to the postsynaptic muscle membrane, although all of the typical synaptic components are present in the mutant. These results indicate that ChAT is uniquely essential for the patterning and formation of mammalian neuromuscular synapses. |
Links | |
Keywords |
Animals; Cell Count; Cell Survival; Choline O-Acetyltransferase/deficiency; Choline O-Acetyltransferase/genetics; Diaphragm/embryology; Diaphragm/innervation; Diaphragm/pathology; Excitatory Postsynaptic Potentials/genetics; Gene Targeting; Mice; Mice, Inbred C57BL; Mice, Mutant Strains; Motor Neurons/pathology; Neuromuscular Diseases/congenital; Neuromuscular Diseases/genetics; Neuromuscular Diseases/pathology; Neuromuscular Junction/pathology; Neuromuscular Junction/ultrastructure; RNA, Messenger/biosynthesis; Receptor Aggregation; Receptors, Cholinergic/genetics; Receptors, Cholinergic/metabolism; Synapses/metabolism; Synapses/ultrastructure; Synaptic Transmission/genetics; Synaptophysin/biosynthesis |
public |
Cancel |