Visual Deprivation Reactivates Rapid Ocular Dominance Plasticity in Adult Visual Cortex

He, Hai-yan; Hodos, William; Quinlan, Elizabeth

doi:10.1523/jneurosci.5554-05.2006

Cited by 233 publications

(243 citation statements)

References 42 publications

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“…Most previous reports of enhanced cortical plasticity have focused on either altering the timing of the developmental critical period or reactivating plasticity in adult animals (5,(23)(24)(25)(26)(27)(28)(29). In contrast, we describe enhanced plasticity at a developmental stage when plasticity is already at its peak.…”

Section: Discussion Acceleration Of Multiple Forms Of Visual Cortex Pmentioning

confidence: 79%

Constitutively active H-ras accelerates multiple forms of plasticity in developing visual cortex

Kaneko

Cheetham

Lee

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Experience-dependent cortical plasticity has been studied by using loss-of-function methods. Here, we take the complementary approach of using a genetic gain-of-function that enhances plasticity. We show that a constitutively active form of H-ras (H-ras G12V ), expressed presynaptically at excitatory synapses in mice, accelerates and enhances multiple, mechanistically distinct forms of plasticity in the developing visual cortex. In vivo, H-ras G12V not only increased the rate of ocular dominance change in response to monocular deprivation (MD), but also accelerated recovery from deprivation by reverse occlusion. In vitro, H-ras G12V expression decreased baseline presynaptic release probability and enhanced presynaptically expressed longterm potentiation (LTP). H-ras G12V expression also accelerated the increase following MD in the frequency of miniature excitatory potentials, mirroring accelerated plasticity in vivo. These findings demonstrate accelerated neocortical plasticity, which offers an avenue toward future therapies for many neurological and neuropsychiatric disorders.gain of function | monocular deprivation | mouse | ocular dominance | presynaptic long-term potentiation

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Section: Discussion Acceleration Of Multiple Forms Of Visual Cortex Pmentioning

confidence: 79%

Constitutively active H-ras accelerates multiple forms of plasticity in developing visual cortex

Kaneko

Cheetham

Lee

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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“…However, the retardation of silent synapse maturation and critical period closure have not been causally linked. Instead, given that dark rearing profoundly influences the properties of neural circuits, including excitatory/ inhibitory balance and metaplasticity (delaying the NMDA receptor subunit switch from GluN2B to GluN2A), other cellular mechanisms have been favored (61)(62)(63)(64)(65). An impaired developmental NMDA receptor subunit switch is unlikely causal for the lack of CP closure in PSD-95 KO mice: Although in young PSD-95 KO mice more synaptic GluN2B-containing NMDA receptors are Table S2. present (35), the synaptic GluN2B levels are not altered in adult PSD-95 KO mice (56).…”

Section: Discussionmentioning

confidence: 99%

Progressive maturation of silent synapses governs the duration of a critical period

Huang

Stodieck

Goetze

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

100

172

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During critical periods, all cortical neural circuits are refined to optimize their functional properties. The prevailing notion is that the balance between excitation and inhibition determines the onset and closure of critical periods. In contrast, we show that maturation of silent glutamatergic synapses onto principal neurons was sufficient to govern the duration of the critical period for ocular dominance plasticity in the visual cortex of mice. Specifically, postsynaptic density protein-95 (PSD-95) was absolutely required for experience-dependent maturation of silent synapses, and its absence before the onset of critical periods resulted in lifelong juvenile ocular dominance plasticity. Loss of PSD-95 in the visual cortex after the closure of the critical period reinstated silent synapses, resulting in reopening of juvenile-like ocular dominance plasticity. Additionally, silent synapse-based ocular dominance plasticity was largely independent of the inhibitory tone, whose developmental maturation was independent of PSD-95. Moreover, glutamatergic synaptic transmission onto parvalbumin-positive interneurons was unaltered in PSD-95 KO mice. These findings reveal not only that PSD-95-dependent silent synapse maturation in visual cortical principal neurons terminates the critical period for ocular dominance plasticity but also indicate that, in general, once silent synapses are consolidated in any neural circuit, initial experience-dependent functional optimization and critical periods end.

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“…73 There is also indirect evidence that the enhanced experience-dependent visual cortical plasticity driven by exposure of adult rats to complete darkness may also be related to a reduced expression of GABAA receptors relative to AMPA receptors, thus altering the balance between inhibition and excitation in the visual cortex. 74,75 Figure 3 Experience-dependent reactivation of neural plasticity in the adult visual cortex. (a) EE in adulthood promotes visual acuity and binocularity recovery from amblyopia.…”

Section: Rejuvenating the Adult Brainmentioning

confidence: 99%

Nurturing brain plasticity: impact of environmental enrichment

et al. 2009

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Environmental enrichment (EE) is known to profoundly affect the central nervous system (CNS) at the functional, anatomical and molecular level, both during the critical period and during adulthood. Recent studies focusing on the visual system have shown that these effects are associated with the recruitment of previously unsuspected neural plasticity processes. At early stages of brain development, EE triggers a marked acceleration in the maturation of the visual system, with maternal behaviour acting as a fundamental mediator of the enriched experience in both the foetus and the newborn. In adult brain, EE enhances plasticity in the cerebral cortex, allowing the recovery of visual functions in amblyopic animals. The molecular substrate of the effects of EE on brain plasticity is multi-factorial, with reduced intracerebral inhibition, enhanced neurotrophin expression and epigenetic changes at the level of chromatin structure. These findings shed new light on the potential of EE as a non-invasive strategy to ameliorate deficits in the development of the CNS and to treat neurological disorders.

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Visual Deprivation Reactivates Rapid Ocular Dominance Plasticity in Adult Visual Cortex

Cited by 233 publications

References 42 publications

Constitutively active H-ras accelerates multiple forms of plasticity in developing visual cortex

Constitutively active H-ras accelerates multiple forms of plasticity in developing visual cortex

Progressive maturation of silent synapses governs the duration of a critical period

Nurturing brain plasticity: impact of environmental enrichment

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