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The Journal of Neuroscience, November 19, 2003, 23(33):10467-10474

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Cellular/Molecular
Optical Measurements of Presynaptic Release in Mutant Zebrafish Lacking Postsynaptic Receptors

Weiyan Li, Fumihito Ono, and Paul Brehm

Department of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, New York 11794

Differentiation of presynaptic nerve terminals is mediated, in part, through contact with the appropriate postsynaptic target cell. In particular, studies using dissociated nerve and muscle derived from Xenopus embryos have indicated that the properties of transmitter release from motor neurons are altered after contact with skeletal muscle. This maturation of presynaptic function has further been linked to retrograde signaling from muscle that involves activation of postsynaptic ACh receptors. Using FM1-43 optical determinants of exocytosis, we now compare calcium-mediated exocytosis at neuromuscular junctions of wild-type zebrafish to mutant fish lacking postsynaptic ACh receptors. In response to either high-potassium depolarization or direct electrical stimulation, we observed no differences in the rate or extent of FM1-43 destaining. These data indicate that the acquisition of stimulus-evoked exocytosis at early developmental stages occurs independent of both postsynaptic receptor and synaptic responses in zebrafish.

Key words: zebrafish; mutant; neuromuscular junction; acetylcholine receptor; motor neuron; presynaptic differentiation; exocytosis

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Received Aug 13, 2003; revised September 12, 2003; accepted September 22, 2003.

This article has been cited by other articles:

				K. E. Epley, J. M. Urban, T. Ikenaga, and F. Ono A Modified Acetylcholine Receptor {delta}-Subunit Enables a Null Mutant to Survive Beyond Sexual Maturation J. Neurosci., December 3, 2008; 28(49): 13223 - 13231. [Abstract] [Full Text] [PDF]

				M. Wang, H. Wen, and P. Brehm Function of Neuromuscular Synapses in the Zebrafish Choline-Acetyltransferase Mutant bajan J Neurophysiol, October 1, 2008; 100(4): 1995 - 2004. [Abstract] [Full Text] [PDF]

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				S. Rassadi, A. Krishnaswamy, B. Pie, R. McConnell, M. H. Jacob, and E. Cooper A Null Mutation for the {alpha}3 Nicotinic Acetylcholine (ACh) Receptor Gene Abolishes Fast Synaptic Activity in Sympathetic Ganglia and Reveals That ACh Output from Developing Preganglionic Terminals Is Regulated in an Activity-Dependent Retrograde Manner J. Neurosci., September 14, 2005; 25(37): 8555 - 8566. [Abstract] [Full Text] [PDF]

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				J. L. Lefebvre, F. Ono, C. Puglielli, G. Seidner, C. Franzini-Armstrong, P. Brehm, and M. Granato Increased neuromuscular activity causes axonal defects and muscular degeneration Development, June 1, 2004; 131(11): 2605 - 2618. [Abstract] [Full Text] [PDF]

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