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Volume 17, Number 19,
Issue of October 1, 1997
pp. 7203-7209
Copyright ©1997 Society for Neuroscience
Evidence That Cysteine String Proteins Regulate an Early Step in
the Ca2+-Dependent Secretion of Neurotransmitter at
Drosophila Neuromuscular Junctions
Received April 29, 1997; revised July 7, 1997; accepted July 10, 1997.
Joy A. Umbach and
Cameron B. Gundersen
Department of Molecular and Medical Pharmacology and The Crump
Institute for Biological Imaging, University of California at Los
Angeles School of Medicine, Los Angeles, California, 90095
Previous work indicated that the temperature-dependent block of
synaptic transmission in cysteine string protein (csp) mutants of
Drosophila was attributable to a failure of nerve
impulses to trigger transmitter release. The current investigations
were undertaken to resolve in more detail the mechanism of this
transmission deficit. Our studies reveal that the spider venom toxin
-latrotoxin can trigger a sustained discharge of quanta at
neuromuscular junctions of csp mutant larvae at
nonpermissive temperature. The same is true of the calcium ionophore
ionomycin. However, solutions with an elevated concentration of K or Ca
ions fail to circumvent the block of quantal secretion in these
mutants. Likewise, 4-aminopyridine, which augments transmitter release
at permissive temperature in csp mutants, fails to
reverse the inhibition of impulse-evoked transmitter release at
elevated temperature. These data are consistent with the hypothesis
that there is a deficit either in Ca ion entry or in the ability of Ca
ions to trigger exocytosis in csp mutants at
nonpermissive temperatures. In part, because of previous work showing
that csps are important for the functional expression of N-type Ca
channels in frog oocytes, we favor the idea that csps participate in a
regulatory interaction involving presynaptic Ca channels.
Key words:
cysteine string proteins;
synaptic transmission;
-latrotoxin;
presynaptic calcium channels;
Drosophila;
shibire
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