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Volume 16, Number 12,
Issue of June 15, 1996
pp. 3877-3886
Copyright ©1996 Society for Neuroscience
Homeostasis of Synaptic Transmission in Drosophila
with Genetically Altered Nerve Terminal Morphology
Received Dec. 15, 1995; revised March 21, 1996; accepted March 25, 1996.
Bryan A. Stewart1,
Christoph M. Schuster2,
Corey S. Goodman2, and
Harold L. Atwood1
1 Department of Physiology, University of Toronto,
Toronto, Ontario, Canada, M5S 1A8, and 2 Howard Hughes
Medical Institute, Department of Cellular and Molecular Biology,
University of California, Berkeley, California 94720
We present a new test of the hypothesis that synaptic strength is
directly related to nerve terminal morphology through analysis of
synaptic transmission at Drosophila neuromuscular junctions
with a genetically reduced number of nerve terminal varicosities.
Synaptic transmission would decrease in target cells with fewer
varicosities if there is a relationship between the number of
varicosities and the strength of synaptic transmission. Animals that
have an extreme hypomorphic allele of the gene for the cell adhesion
molecule Fasciclin II possess fewer synapse-bearing nerve terminal
varicosities; nevertheless, synaptic strength is maintained at a normal
level for the muscle cell as a whole. Fewer failures of
neurotransmitter release and larger excitatory junction potentials from
individual varicosities, as well as more frequent spontaneous release
and larger quantal units, provide evidence for enhancement of
transmitter release from varicosities in the mutant. Ultrastructural
analysis reveals that mutant nerve terminals have bigger synapses with
more active zones per synapse, indicating that synaptic enlargement and
an accompanying increase in synaptic complexity provide for more
transmitter release at mutant varicosities. These results show that
morphological parameters of transmitting nerve terminals can be
adjusted to functionally compensate for genetic perturbations, thereby
maintaining optimal synaptic transmission.
Key words:
synaptic transmission;
neuromuscular junction;
electron microscopy;
ultrastructure;
cell adhesion molecule;
Fasciclin
II
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