Research ResourceNeuroscience

Remodeling of the Homer-Shank interactome mediates homeostatic plasticity

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Science Signaling  04 May 2021:
Vol. 14, Issue 681, eabd7325
DOI: 10.1126/scisignal.abd7325

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Stabilized by protein interactions

Synaptic scaling is a homeostatic plasticity mechanism in which neuronal excitability is stabilized despite prolonged changes in synaptic input through compensatory adjustments in the strength of the connections between neurons. Heavner et al. built an activity-regulated postsynaptic protein interaction network (PIN) in mice. This PIN changed differentially to prolonged increases in activity compared to prolonged decreases and to the activity manipulations performed in culture compared to those performed in vivo. Some of the changes in this PIN did not occur in mice lacking either Homer1 or Shank3, scaffolding protein–encoding genes that are mutated in some patients with autism spectrum disorder. The findings begin to elucidate the complexity and context dependence of homeostatic synaptic plasticity and create a framework for exploring whether these changes contribute to autism and associated disorders in patients.

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