scholarly journals Arg206 of SNAP-25 is essential for neuroexocytosis at the Drosophila melanogaster neuromuscular junction

2010 ◽  
Vol 123 (19) ◽  
pp. 3276-3283 ◽  
Author(s):  
A. Megighian ◽  
M. Scorzeto ◽  
D. Zanini ◽  
S. Pantano ◽  
M. Rigoni ◽  
...  
2013 ◽  
Vol 200 (2) ◽  
pp. 219-233 ◽  
Author(s):  
Keisuke Kamimura ◽  
Kohei Ueno ◽  
Jun Nakagawa ◽  
Rie Hamada ◽  
Minoru Saitoe ◽  
...  

Heparan sulfate proteoglycans (HSPGs) play pivotal roles in the regulation of Wnt signaling activity in several tissues. At the Drosophila melanogaster neuromuscular junction (NMJ), Wnt/Wingless (Wg) regulates the formation of both pre- and postsynaptic structures; however, the mechanism balancing such bidirectional signaling remains elusive. In this paper, we demonstrate that mutations in the gene of a secreted HSPG, perlecan/trol, resulted in diverse postsynaptic defects and overproduction of synaptic boutons at NMJ. The postsynaptic defects, such as reduction in subsynaptic reticulum (SSR), were rescued by the postsynaptic activation of the Frizzled nuclear import Wg pathway. In contrast, overproduction of synaptic boutons was suppressed by the presynaptic down-regulation of the canonical Wg pathway. We also show that Trol was localized in the SSR and promoted postsynaptic accumulation of extracellular Wg proteins. These results suggest that Trol bidirectionally regulates both pre- and postsynaptic activities of Wg by precisely distributing Wg at the NMJ.


2017 ◽  
Author(s):  
Catherine J. Yeates ◽  
C. Andrew Frank

ABSTRACTHomeostasis is a vital mode of biological self-regulation. The hallmarks of homeostasis for any biological system are a baseline set point of physiological activity, detection of unacceptable deviations from the set point, and effective corrective measures to counteract deviations. Homeostatic synaptic plasticity (HSP) is a form of neuroplasticity in which neurons and circuits resist environmental perturbations in order to maintain appropriate levels of activity. One assumption is that if an environmental perturbation triggers homeostatic corrective changes in neuronal properties, those corrective measures should be reversed upon removal of the perturbation. We test the reversibility and limits of HSP at a well-studied model synapse, the Drosophila melanogaster neuromuscular junction (NMJ). At the Drosophila NMJ, impairment of glutamate receptors causes a decrease in quantal size, which is offset by a corrective, homeostatic increase in the number of vesicles released per evoked presynaptic stimulus, or quantal content. This process has been termed presynaptic homeostatic potentiation (PHP). Taking advantage of a GAL4/GAL80TS/UAS expression system, we triggered PHP by expressing a dominant-negative glutamate receptor subunit at the NMJ. We then reversed PHP by halting expression of the dominant-negative receptor. Our data show that PHP is fully reversible over a time course of 48-72 hours after the dominant-negative glutamate receptor stops being genetically expressed. Additionally, we found that the PHP response triggered by the dominant-negative subunit was ablated at high temperatures. Our data show that the long-term maintenance of PHP at the Drosophila NMJ is a reversible regulatory process that is sensitive to temperature.SIGNIFICANCE STATEMENTBiological homeostatic systems must upregulate or downregulate cellular parameters in order to maintain appropriate set points of physiological activity. Homeostasis is a well-documented mode of regulation in metazoan nervous systems. True homeostatic control should be a reversible process – but due to technical difficulties of presenting and removing functional challenges to living synapses, the reversibility of homeostatic forms of synapse regulation has not been rigorously examined in vivo over extended periods of developmental time. Here we formally demonstrate that homeostatic regulation of Drosophila melanogaster neuromuscular synapse function is reversible and temperature-labile. This is significant because developing methods to study how homeostatic regulatory systems are turned on and off could lead to fundamental new insights about control of synaptic output.


PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e68385 ◽  
Author(s):  
Katherine R. Nesler ◽  
Robert I. Sand ◽  
Breanna A. Symmes ◽  
Sarala J. Pradhan ◽  
Nathan G. Boin ◽  
...  

1988 ◽  
Vol 66 (3) ◽  
pp. 321-327 ◽  
Author(s):  
James G. McLarnon ◽  
David M. J. Quastel

The point and single electrode voltage clamp methods have been used to study the characteristics of junctional currents in Drosophila melanogaster larvae muscle fibers and the modulation of these currents by excitatory amino acids, short and long chain n-alkanols, and pentobarbital. The decay phase of junctional currents in Drosophila was found to be dominated by cooperativity in transmitter binding associated with reverberation, that is, repeated binding of transmitter with receptors as the transmitter molecules diffuse away from the active region. The current decay does not directly reflect the closure of ion channels and is qualitatively similar to the decay of miniature end-plate currents at the mouse neuromuscular junction after poisoning of acetylcholinesterase by paraoxon. In Drosophila an increase in membrane hyperpolarization both slows the time course of current decay and increases the degree of reverberation. The application of excitatory amino acids including glutamate, N-methyl-D-aspartate, quisqualate, and kainate causes a significant decrease in the amplitude of the junctional currents, a prolongation of the decay time course, and a reduction in reverberation of transmitter. The height of junctional currents is also diminished by the n-alkanols ethanol, pentanol, and octanol and by the barbiturate pentobarbital; ethanol also hastened the time course of decay of the currents.


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