Slow-channel transgenic mice: A model of postsynaptic organellar degeneration at the neuromuscular junction

Journal of Neuroscience

Volumn 17, Issue 11, 1997, Pages 4170-4179

  Gomez, Christopher M ^a   Maselli, Ricardo ^b   Gundeck, Jo Ellen ^a   Chao, Mary ^b   Day, John W ^a   Tamamizu, Shiori ^b   Lasalde, Jose A ^b,d   McNamee, Mark ^b   Wollmann, Robert L ^c  

^a UNIVERSITY OF MINNESOTA   (United States)

^b UNIVERSITY OF CALIFORNIA   (United States)

^c UNIVERSITY OF CHICAGO   (United States)

^d UNIVERSITY OF PUERTO RICO   (Puerto Rico)

Author keywords

acetylcholine receptor; calcium overload; excitotoxicity; neuromuscular junction; point mutation; slow channel congenital myasthenic syndrome; synaptic degeneration; transgenic mice

Indexed keywords

CALCIUM; CHOLINERGIC RECEPTOR; ION CHANNEL;

ADOLESCENT; ANIMAL CELL; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL DEGENERATION; CONTROLLED STUDY; EMBRYO; ENDPLATE POTENTIAL; GENE EXPRESSION; HUMAN; MOUSE; MYASTHENIA; NEUROMUSCULAR JUNCTION DISORDER; NONHUMAN; POINT MUTATION; PRIORITY JOURNAL; TRANSGENIC MOUSE; XENOPUS;

EID: 0030905263     PISSN: 02706474     EISSN: None     Source Type: Journal    
DOI: 10.1523/jneurosci.17-11-04170.1997     Document Type: Article

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