Autor: |
Ono F; Department of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, New York 11794, USA., Shcherbatko A, Higashijima S, Mandel G, Brehm P |
Jazyk: |
angličtina |
Zdroj: |
The Journal of neuroscience : the official journal of the Society for Neuroscience [J Neurosci] 2002 Aug 01; Vol. 22 (15), pp. 6491-8. |
DOI: |
20026669 |
Abstrakt: |
Upon touch, twitch once zebrafish respond with one or two swimming strokes instead of typical full-blown escapes. This use-dependent fatigue is shown to be a consequence of a mutation in the tetratricopeptide domain of muscle rapsyn, inhibiting formation of subsynaptic acetylcholine receptor clusters. Physiological analysis indicates that reduced synaptic strength, attributable to loss of receptors, is augmented by a potent postsynaptic depression not seen at normal neuromuscular junctions. The synergism between these two physiological processes is causal to the use-dependent muscle fatigue. These findings offer insights into the physiological basis of human myasthenic syndrome and reveal the first demonstration of a role for rapsyn in regulating synaptic function. |
Databáze: |
MEDLINE |
Externí odkaz: |
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