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The Journal of Neurophysiology Vol. 82 No. 1 July 1999, pp. 123-130
Copyright ©1999 by the American Physiological Society
Department of Biology, The Pennsylvania State University, University Park, Pennsylvania 16802
Kawasaki, Fumiko and
Richard W. Ordway.
The Drosophila NSF Protein, dNSF1, Plays a
Similar Role at Neuromuscular and Some Central Synapses. J. Neurophysiol. 82: 123-130, 1999.
The
N-ethylmaleimide sensitive fusion protein (NSF) was
originally identified as a cytosolic factor required for constitutive vesicular transport and later implicated in synaptic vesicle
trafficking as well. Our previous work at neuromuscular synapses in the
temperature-sensitive NSF mutant, comatose
(comt), has shown that the comt
gene product, dNSF1, functions after synaptic vesicle docking in the
priming of vesicles for fast calcium-triggered fusion. Here we
investigate whether dNSF1 performs a similar function at central
synapses associated with the well-characterized giant fiber neural
pathway. These include a synapse within the giant fiber pathway, made
by the peripherally synapsing interneuron (PSI), as well as synapses providing input to the giant fiber pathway. The latency (delay) between
stimulation and a resulting muscle action potential was used to assess
the function of each class of synapses. Repetitive stimulation of the
giant fiber pathway in comt produced wild-type responses
at both 20 and 36°C, exhibiting a characteristic and constant latency
between stimulation and the muscle response. In contrast, stimulation
of presynaptic inputs to the giant fiber (referred to as the "long
latency pathway") revealed a striking difference between wild type
and comt at 36°C. Repetitive stimulation of the long
latency pathway led to a progressive, activity-dependent increase in
the response latency in comt, but not in wild type. Thus
the giant fiber pathway, including the PSI synapse, appears to function
normally in comt, whereas the presynaptic inputs to the
giant fiber pathway are disrupted. Several aspects of the progressive
latency increase observed in the long latency pathway can be understood
in the context of the activity-dependent reduction in neurotransmitter
release we observed previously at neuromuscular synapses. These results
suggest that repetitive stimulation causes a progressive reduction in
neurotransmitter release by presynaptic inputs to the giant fiber
neuron, resulting in an increased latency preceding a giant fiber
action potential. Thus synapses presynaptic to the giant fiber appear
to utilize dNSF1 in a manner similar to the neuromuscular synapse,
whereas the PSI chemical synapse may differ with respect to the
expression or activity of dNSF1.
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