title: Elimination of inhibitory synapses is a major component of adult ocular dominance plasticity.
abstract: During development, cortical plasticity is associated with the rearrangement of excitatory connections. While these connections become more stable with age, plasticity can still be induced in the adult cortex. Here we provide evidence that structural plasticity of inhibitory synapses onto pyramidal neurons is a major component of plasticity in the adult neocortex. In vivo two-photon imaging was used to monitor the formation and elimination of fluorescently labeled inhibitory structures on pyramidal neurons. We find that ocular dominance plasticity in the adult visual cortex is associated with rapid inhibitory synapse loss, especially of those present on dendritic spines. This occurs not only with monocular deprivation but also with subsequent restoration of binocular vision. We propose that in the adult visual cortex the experience-induced loss of inhibition may effectively strengthen specific visual inputs with limited need for rearranging the excitatory circuitry.
authors.affiliation: Department of Molecular Visual Plasticity, Netherlands Institute for Neuroscience, an Institute of the Royal Netherlands Academy of Arts and Sciences, Meibergdreef 47, 1105 BA Amsterdam, The Netherlands.
authors.forename: Daniëlle
authors.initials: D
authors.lastname: van Versendaal
authors.forename: Rajeev
authors.initials: R
authors.lastname: Rajendran
authors.forename: M Hadi
authors.initials: MH
authors.lastname: Saiepour
authors.forename: Jan
authors.initials: J
authors.lastname: Klooster
authors.forename: Laura
authors.initials: L
authors.lastname: Smit-Rigter
authors.forename: Jean-Pierre
authors.initials: JP
authors.lastname: Sommeijer
authors.forename: Chris I
authors.initials: CI
authors.lastname: De Zeeuw
authors.forename: Sonja B
authors.initials: SB
authors.lastname: Hofer
authors.forename: J Alexander
authors.initials: JA
authors.lastname: Heimel
authors.forename: Christiaan N
authors.initials: CN
authors.lastname: Levelt
mesh_terms: D000367:Age Factors; D000818:Animals; D002352:Carrier Proteins / Q000235:genetics; D049229:Dendritic Spines / Q000378:metabolism / Q000648:ultrastructure; D023882:Dominance, Ocular / Q000502:physiology*; D018274:Electroporation; D049452:Green Fluorescent Proteins / Q000235:genetics; D066298:In Vitro Techniques; D008164:Luminescent Proteins / Q000235:genetics; D008565:Membrane Proteins / Q000235:genetics; D051379:Mice; D046529:Microscopy, Electron, Transmission; D009433:Neural Inhibition / Q000235:genetics / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000502:physiology* / Q000648:ultrastructure; D012683:Sensory Deprivation; D013569:Synapses / Q000502:physiology* / Q000648:ultrastructure; D013997:Time Factors; D050599:Vesicular Glutamate Transport Protein 2 / Q000378:metabolism; D050495:Vesicular Inhibitory Amino Acid Transport Proteins / Q000378:metabolism; D014793:Visual Cortex / Q000166:cytology*; D014795:Visual Pathways / Q000502:physiology
chemical_list: D002352:Carrier Proteins; D008164:Luminescent Proteins; D008565:Membrane Proteins; C493477:Slc17a6 protein, mouse; D050599:Vesicular Glutamate Transport Protein 2; D050495:Vesicular Inhibitory Amino Acid Transport Proteins; C492244:Viaat protein, mouse; C413663:fluorescent protein 583; C073441:gephyrin; D049452:Green Fluorescent Proteins