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Fig. 4. twister-related nerve and muscle defects are caused by prolonged
synaptic transmission. (A) Injecting buffer into embryos obtained from two
twister heterozygotes resulted in the expected distribution of axonal
and muscle phenotypes, i.e. 75% displayed wild-type or heterozygous axonal and
myofiber phenotypes (white bar), whereas 25% displayed severe axonal and
myofiber defects (gray bar; n=261, from three experiments). In
contrast, 
-BTX injection increased the proportion of embryos displaying
wild-type or heterozygous axonal and myofiber morphology (88.1±3.2%),
and decreased the proportion of embryos displaying twister homozygous
defects (11.9±3.2%; n=475 from six experiments;
P<0.0001 for Fisher's exact test). (B-G) Comparison of spontaneous
(mEPC) and evoked (EPC) synaptic currents obtained by whole-cell voltage clamp
of 72 hpf wild-type (B) and heterozygous twister (C) larvae. (B,C)
The plot represents the average of 10 individual spontaneous currents, aligned
at the peaks. (D,E) Frequency histograms of decay times for individual mEPCs
from wild-type (D) and heterozygous twister (E) muscle. Decay times
were determined on the basis of 90% decay from peak amplitude. Note that in
wild-type muscle, all events showed decay times shorter or equal to 10
mseconds, whereas in mutant muscle most of the events had decay times longer
than 10 mseconds (black arrows). (F,G) Evoked end-plate currents obtained from
wild-type (F) and heterozygous twister (G) muscle in response to 50
Hz stimulation of the spinal cord. Ten consecutive trains were averaged. Time
points of stimulation are indicated by filled circles and the broken line
indicates the baseline holding current.
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