The role of cAMP in synaptic homeostasis in response to environmental temperature challenges and hyperexcitability mutations.
The role of cAMP in synaptic homeostasis in response to environmental temperature challenges and hyperexcitability mutations.
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DOI:
10.3389/fncel.2015.00010
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发表时间:
2015
影响因子:
5.3
通讯作者:
Wu CF
中科院分区:
文献类型:
--
作者:
Ueda A;Wu CF
Homeostasis is the ability of physiological systems to regain functional balance following environment or experimental insults and synaptic homeostasis has been demonstrated in various species following genetic or pharmacological disruptions. Among environmental challenges, homeostatic responses to temperature extremes are critical to animal survival under natural conditions. We previously reported that axon terminal arborization in Drosophila larval neuromuscular junctions (NMJs) is enhanced at elevated temperatures; however, the amplitude of excitatory junctional potentials (EJPs) remains unaltered despite the increase in synaptic bouton numbers. Here we determine the cellular basis of this homeostatic adjustment in larvae reared at high temperature (HT, 29°C). We found that synaptic current focally recorded from individual synaptic boutons was unaffected by rearing temperature (<15°C to >30°C). However, HT rearing decreased the quantal size (amplitude of spontaneous miniature EJPs, or mEJPs), which compensates for the increased number of synaptic releasing sites to retain a normal EJP size. The quantal size decrease is accounted for by a decrease in input resistance of the postsynaptic muscle fiber, indicating an increase in membrane area that matches the synaptic growth at HT. Interestingly, a mutation in rutabaga (rut) encoding adenylyl cyclase (AC) exhibited no obvious changes in quantal size or input resistance of postsynaptic muscle cells after HT rearing, suggesting an important role for rut AC in temperature-induced synaptic homeostasis in Drosophila. This extends our previous finding of rut-dependent synaptic homeostasis in hyperexcitable mutants, e.g., slowpoke (slo). In slo larvae, the lack of BK channel function is partially ameliorated by upregulation of presynaptic Shaker (Sh) IA current to limit excessive transmitter release in addition to postsynaptic glutamate receptor recomposition that reduces the quantal size.
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DOI:
10.1523/jneurosci.4701-09.2010
发表时间:
2010-02-03
期刊:
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子:
--
作者:
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发表时间:
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影响因子:
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作者:
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通讯作者:
PROSSER, CL
影响因子:
2.5
作者:
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通讯作者:
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DOI:
10.1073/pnas.0400773101
发表时间:
2004-03-23
影响因子:
11.1
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通讯作者:
Rössler, W
影响因子:
1.9
作者:
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通讯作者:
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