Persistent Electrical Coupling and Locomotory Dysfunction in the Zebrafish Mutant shocked

• Published in: Journal of neurophysiology Vol. 92; no. 4; pp. 2003 - 2009
• Main Authors: Luna, Victor M, Wang, Meng, Ono, Fumihito, Gleason, Michelle R, Dallman, Julia E, Mandel, Gail, Brehm, Paul
• Format: Journal Article
• Language: English
• Published: United States Am Phys Soc 01.10.2004
• Subjects: Animals; Connexin 43 - genetics; Connexin 43 - physiology; Connexins - genetics; Connexins - physiology; Danio rerio; Electrophysiology; Evoked Potentials - physiology; Freshwater; Locomotion - genetics; Locomotion - physiology; Mutation - physiology; Nervous System Diseases - genetics; Nervous System Diseases - physiopathology; Patch-Clamp Techniques; Phenotype; Zebrafish - genetics; Zebrafish - physiology
• DOI: 10.1152/jn.00454.2004
• ISSN: 0022-3077

1 Department of Neurobiology and Behavior and 2 Howard Hughes Medical Institute, State University of New York, Stony Brook, New York 11794 Submitted 3 May 2004; accepted in final form 8 June 2004 On initial formation of neuromuscular junctions, slow synaptic signals interact through an electrically coupled network of muscle cells. After the developmental onset of muscle excitability and the transition to fast synaptic responses, electrical coupling diminishes. No studies have revealed the functional importance of the electrical coupling or its precisely timed loss during development. In the mutant zebrafish shocked ( sho ) electrical coupling between fast muscle cells persists beyond the time that it would normally disappear in wild-type fish. Recordings from sho indicate that muscle depolarization in response to motor neuron stimulation remains slow due to the low-pass filter characteristics of the coupled network of muscle cells. Our findings suggest that the resultant prolonged muscle depolarizations contribute to the premature termination of swimming in sho and the delayed acquisition of the normally rapid touch-triggered movements. Thus the benefits of gap junctions during early synapse development likely become a liability if not inactivated by the time that muscle would normally achieve fast autonomous function. Address for reprint requests and other correspondence: P. Brehm, Dept. of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, NY 11794 (E-mail: pbrehm{at}notes.cc.sunysb.edu ).