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