title: Homeostatic plasticity mechanisms in mouse V1.
abstract: Mechanisms thought of as homeostatic must exist to maintain neuronal activity in the brain within the dynamic range in which neurons can signal. Several distinct mechanisms have been demonstrated experimentally. Three mechanisms that act to restore levels of activity in the primary visual cortex of mice after occlusion and restoration of vision in one eye, which give rise to the phenomenon of ocular dominance plasticity, are discussed. The existence of different mechanisms raises the issue of how these mechanisms operate together to converge on the same set points of activity.This article is part of the themed issue 'Integrating Hebbian and homeostatic plasticity'.
authors.affiliation: Center for Integrative Neuroscience and Department of Physiology, University of California, San Francisco, CA 94143-0444, USA.
authors.forename: Megumi
authors.initials: M
authors.lastname: Kaneko
authors.affiliation: Center for Integrative Neuroscience and Department of Physiology, University of California, San Francisco, CA 94143-0444, USA stryker@phy.ucsf.edu.
authors.forename: Michael P
authors.identifier: 0000-0003-1546-5831
authors.initials: MP
authors.lastname: Stryker
mesh_terms: D000818:Animals; D023882:Dominance, Ocular; D006706:Homeostasis; D051379:Mice; D009473:Neuronal Plasticity; D014785:Vision, Ocular; D014793:Visual Cortex / Q000502:physiology*
keywords: TNFα; cortical plasticity; critical period; homeostatic; mouse V1; visual cortex