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Neuron. 2014 Oct 22;84(2):497-510. doi: 10.1016/j.neuron.2014.09.036. Epub 2014 Oct 22.

Modeling the dynamic interaction of Hebbian and homeostatic plasticity.

Author information

1
RIKEN Brain Science Institute, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan; Center for Theoretical Neuroscience and Department of Neuroscience, College of Physicians and Surgeons, Columbia University, 1051 Riverside Drive, New York, NY 10032, USA; Deptartment of Computational Intelligence and Systems Science, Tokyo Institute of Technology, Yokohama 226-8502, Japan. Electronic address: taro.toyoizumi@brain.riken.jp.
2
Center for Integrative Neuroscience and Department of Physiology, University of California, 675 Nelson Rising Lane, San Francisco, San Francisco, CA 94158, USA.
3
Center for Theoretical Neuroscience and Department of Neuroscience, College of Physicians and Surgeons, Columbia University, 1051 Riverside Drive, New York, NY 10032, USA; Kavli Institute for Brain Science, Columbia University, 1051 Riverside Drive, New York, NY 10032, USA.

Abstract

Hebbian and homeostatic plasticity together refine neural circuitry, but their interactions are unclear. In most existing models, each form of plasticity directly modifies synaptic strength. Equilibrium is reached when the two are inducing equal and opposite changes. We show that such models cannot reproduce ocular dominance plasticity (ODP) because negative feedback from the slow homeostatic plasticity observed in ODP cannot stabilize the positive feedback of fast Hebbian plasticity. We propose a model in which synaptic strength is the product of a synapse-specific Hebbian factor and a postsynaptic-cell-specific homeostatic factor, with each factor separately arriving at a stable inactive state. This model captures ODP dynamics and has plausible biophysical substrates. We confirm model predictions experimentally that plasticity is inactive at stable states and that synaptic strength overshoots during recovery from visual deprivation. These results highlight the importance of multiple regulatory pathways for interactions of plasticity mechanisms operating over separate timescales.

PMID:
25374364
PMCID:
PMC4223656
DOI:
10.1016/j.neuron.2014.09.036
[Indexed for MEDLINE]
Free PMC Article

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