PUBLICATION
Persistent electrical coupling and locomotory dysfunction in the zebrafish mutant shocked
- Authors
- Luna, V.M., Wang, M., Ono, F., Gleason, M.R., Dallman, J.E., Mandel, G., and Brehm, P.
- ID
- ZDB-PUB-040621-2
- Date
- 2004
- Source
- Journal of neurophysiology 92(4): 2003-2009 (Journal)
- Registered Authors
- Dallman, Julia, Gleason, Michelle, Ono, Fumihito
- Keywords
- none
- MeSH Terms
-
- Animals
- Connexin 43/genetics
- Connexin 43/physiology
- Connexins/genetics
- Connexins/physiology
- Electrophysiology
- Evoked Potentials/physiology
- Locomotion/genetics*
- Locomotion/physiology*
- Mutation/physiology*
- Nervous System Diseases/genetics*
- Nervous System Diseases/physiopathology*
- Patch-Clamp Techniques
- Phenotype
- Zebrafish/genetics*
- Zebrafish/physiology*
- PubMed
- 15201312 Full text @ J. Neurophysiol.
Citation
Luna, V.M., Wang, M., Ono, F., Gleason, M.R., Dallman, J.E., Mandel, G., and Brehm, P. (2004) Persistent electrical coupling and locomotory dysfunction in the zebrafish mutant shocked. Journal of neurophysiology. 92(4):2003-2009.
Abstract
Upon initial formation of neuromuscular junctions, slow synaptic signals interact through an electrically coupled network of muscle cells. Following 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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping