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Previous Article | Next Article
The Journal of Neuroscience, August 1, 2001, 21(15):5439-5448
Paralytic Zebrafish Lacking Acetylcholine Receptors Fail to Localize Rapsyn Clusters to the Synapse
Fumihito Ono1, Shin-ichi Higashijima1, 2, 3, Anatoly Shcherbatko1, Joseph R. Fetcho1, and Paul Brehm1 1 Department of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, New York 11794, 2 Precursory Research for Embryonic Science and Technology, Japan Science and Technology Corporation, Tokyo, Japan 332-0012, and 3 National Institute for Basic Biology, Okazaki, Japan 351-0198
Physiological analysis of two lines of paralytic mutant zebrafish, relaxed and sofa potato, reveals defects in distinct types of receptors in skeletal muscle. In sofa potato the paralysis results from failed synaptic transmission because of the absence of acetylcholine receptors, whereas relaxed mutants lack dihydropyridine receptor-mediated release of internal calcium in response to the muscle action potential. Synaptic structure and function appear normal in relaxed, showing that muscle paralysis per se does not impede proper synapse development. However, sofa potato mutants show incomplete development of the postsynaptic complex. Specifically, in the absence of ACh receptors, clusters of the receptor-aggregating protein rapsyn form in the extrasynaptic membrane but generally fail to localize to the subsynaptic region. Our results indicate that, although rapsyn molecules are capable of self-aggregation, interaction with ACh receptors is required for proper subsynaptic localization.
Key words: zebrafish; mutant; neuromuscular junction; acetylcholine receptor; dihydropyridine receptor; rapsyn; clustering
Copyright © 2001 Society for Neuroscience 0270-6474/01/21155439-10$05.00/0
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