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Interactions between synaptic homeostatic mechanisms: An attempt to reconcile BCM theory, synaptic scaling, and changing excitation/inhibition balance

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Hübener,  Mark
Department: Synapses-Circuits-Plasticity / Bonhoeffer, MPI of Neurobiology, Max Planck Society;

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Bonhoeffer,  Tobias
Department: Synapses-Circuits-Plasticity / Bonhoeffer, MPI of Neurobiology, Max Planck Society;

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Citation

Keck, T., Hübener, M., & Bonhoeffer, T. (2017). Interactions between synaptic homeostatic mechanisms: An attempt to reconcile BCM theory, synaptic scaling, and changing excitation/inhibition balance. Current Opinion in Neurobiology, 43, 87-93. doi:10.1016/j.conb.2017.02.003.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002D-A609-B
Abstract
Homeostatic plasticity is proposed to be mediated by synaptic changes, such as synaptic scaling and shifts in the excitation/inhibition balance. These mechanisms are thought to be separate from the Bienenstock, Cooper, Munro (BCM) learning rule, where the threshold for the induction of long-term potentiation and long-term depression slides in response to changes in activity levels. Yet, both sets of mechanisms produce a homeostatic response of a relative increase (or decrease) in strength of excitatory synapses in response to overall activity-level changes. Here we review recent studies, with a focus on in vivo experiments, to re-examine the overlap and differences between these two mechanisms and we suggest how they may interact to facilitate firing-rate homeostasis, while maintaining functional properties of neurons.