Upward synaptic scaling is dependent on neurotransmission rather than spiking
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Fong-2015-Upward Synaptic Scaling.pdf
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5.49 MB
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Author(s)
Fong, Ming-fai
Newman, Jonathan P.
Potter, Steve M.
Wenner, Peter
Date Issued
March 2015
Journal
Nature Communications
Publisher
Nature Publishing Group
Citation
Fong, Ming-fai, Jonathan P. Newman, Steve M. Potter, and Peter Wenner. “Upward Synaptic Scaling Is Dependent on Neurotransmission Rather Than Spiking.” Nature Communications 6 (March 9, 2015): 6339.
Version
Final published version
Abstract
Homeostatic plasticity encompasses a set of mechanisms that are thought to stabilize firing rates in neural circuits. The most widely studied form of homeostatic plasticity is upward synaptic scaling (upscaling), characterized by a multiplicative increase in the strength of excitatory synaptic inputs to a neuron as a compensatory response to chronic reductions in firing rate. While reduced spiking is thought to trigger upscaling, an alternative possibility is that reduced glutamatergic transmission generates this plasticity directly. However, spiking and neurotransmission are tightly coupled, so it has been difficult to determine their independent roles in the scaling process. Here we combined chronic multielectrode recording, closed-loop optogenetic stimulation, and pharmacology to show that reduced glutamatergic transmission directly triggers cell-wide synaptic upscaling. This work highlights the importance of synaptic activity in initiating signalling cascades that mediate upscaling. Moreover, our findings challenge the prevailing view that upscaling functions to homeostatically stabilize firing rates.
MIT Department
Picower Institute for Learning and Memory
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Creative Commons Attribution
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DOI of Published Version
https://doi.org/10.1038/ncomms7339
