Environmental Enrichment Promotes Plasticity and Visual Acuity Recovery in Adult Monocular Amblyopic Rats

Tognini, Paola; Manno, Ilaria; Bonaccorsi, Joyce; Cenni, Maria Cristina; Sale, Alessandro; Maffei, Lamberto

doi:10.1371/journal.pone.0034815

Cited by 39 publications

(36 citation statements)

References 29 publications

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“…Various manipulations of sensory environment or experience coupled with physical activity have been shown to recover visual function (Kaneko and Stryker, 2014; Montey et al, 2013; Tognini et al, 2012). These manipulations, however, are likely to have widespread effects in the brain.…”

Section: Discussionmentioning

confidence: 99%

“…Several manipulations have been used to recover visual function in impaired rodents (Kaneko and Stryker, 2014; Maya Vetencourt et al, 2008; Montey et al, 2013; Stephany et al, 2014; Tognini et al, 2012), but none have been shown to restore visual perception using a focal manipulation of plasticity in visual cortex. Here we use a behavioral test to demonstrate that inhibitory neuron transplantation restores the visual perceptual thresholds of impaired mice to normal levels.…”

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confidence: 99%

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Inhibitory Neuron Transplantation into Adult Visual Cortex Creates a New Critical Period that Rescues Impaired Vision

Davis

Velez

Guevarra

et al. 2015

Neuron

129

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The maturation of inhibitory circuits in the juvenile cortex triggers a critical period of plasticity in visual system development. Although several manipulations of inhibition can alter its timing, none have reactivated critical period plasticity in adulthood. We developed a transplantation method to reactivate critical period plasticity in the adult visual cortex. Transplanted embryonic inhibitory neurons from the medial ganglionic eminence reinstate ocular dominance plasticity in adult recipients. Transplanted inhibitory cells develop cell-type appropriate molecular characteristics and visually evoked responses. In adult mice impaired by deprivation during the juvenile critical period, transplantation also recovers both visual cortical responses and performance on a behavioral test of visual acuity. Plasticity and recovery are induced when the critical period would have occurred in the donor animal. These results reveal that the focal reactivation of visual cortical plasticity using inhibitory cell transplantation creates a new critical period that restores visual perception after childhood deprivation.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Inhibitory Neuron Transplantation into Adult Visual Cortex Creates a New Critical Period that Rescues Impaired Vision

Davis

Velez

Guevarra

et al. 2015

Neuron

129

View full text Add to dashboard Cite

show abstract

“…Moreover, BDNF overexpression can rescue visual deprivation that results from dark rearing (Gianfranceschi et al, 2003); phenomenon that is often associated with prolonging the critical period for ocular dominance plasticity. Recent studies have demonstrated that recovery of visual acuity in adult amblyopic rats by environmental enrichment is also associated with an increase in expression of BDNF (Tognini et al, 2012). Although other cellular proteins also change due to environmental enrichment, changes in BDNF reinforce the earlier studies that report the modulatory role of BDNF in critical period plasticity.…”

Section: Physiology and Behaviormentioning

confidence: 99%

Consequences of brain-derived neurotrophic factor withdrawal in CNS neurons and implications in disease

Mariga

Mitre

Chao

2017

Neurobiology of Disease

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Growth factor withdrawal has been studied across different species and has been shown to have dramatic consequences on cell survival. In the nervous system, withdrawal of nerve growth factor (NGF) from sympathetic and sensory neurons results in substantial neuronal cell death, signifying a requirement for NGF for the survival of neurons in the peripheral nervous system (PNS). In contrast to the PNS, withdrawal of central nervous system (CNS) enriched brain-derived neurotrophic factor (BDNF) has little effect on cell survival but is indispensible for synaptic plasticity. Given that most early events in neuropsychiatric disorders are marked by a loss of synapses, lack of BDNF may thus be an important part of a cascade of events that leads to neuronal degeneration. Here we review reports on the effects of BDNF withdrawal on CNS neurons and discuss the relevance of the loss in disease.

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“…As a consequence, many researches are focused to find treatments for adult subjects. Since the long-term MD results in permanent loss of visual acuity (amblyopia; Morishita and Hensch, 2008), prolonged MD has become soon a classical model to study modifications triggered by compromised binocular inputs and a protocol in order to test therapeutic treatment, especially in the adult brain (Sale et al, 2007; Sengpiel, 2011; Spolidoro et al, 2011; Baroncelli et al, 2012; Tognini et al, 2012). …”

Section: Callosal Plasticity: How Visual Input Impacts On Interhemispmentioning

confidence: 99%

Reorganization of Visual Callosal Connections Following Alterations of Retinal Input and Brain Damage

Restani

Caleo

2016

Front. Syst. Neurosci.

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Vision is a very important sensory modality in humans. Visual disorders are numerous and arising from diverse and complex causes. Deficits in visual function are highly disabling from a social point of view and in addition cause a considerable economic burden. For all these reasons there is an intense effort by the scientific community to gather knowledge on visual deficit mechanisms and to find possible new strategies for recovery and treatment. In this review, we focus on an important and sometimes neglected player of the visual function, the corpus callosum (CC). The CC is the major white matter structure in the brain and is involved in information processing between the two hemispheres. In particular, visual callosal connections interconnect homologous areas of visual cortices, binding together the two halves of the visual field. This interhemispheric communication plays a significant role in visual cortical output. Here, we will first review the essential literature on the physiology of the callosal connections in normal vision. The available data support the view that the callosum contributes to both excitation and inhibition to the target hemisphere, with a dynamic adaptation to the strength of the incoming visual input. Next, we will focus on data showing how callosal connections may sense visual alterations and respond to the classical paradigm for the study of visual plasticity, i.e., monocular deprivation (MD). This is a prototypical example of a model for the study of callosal plasticity in pathological conditions (e.g., strabismus and amblyopia) characterized by unbalanced input from the two eyes. We will also discuss the findings of callosal alterations in blind subjects. Noteworthy, we will discuss data showing that inter-hemispheric transfer mediates recovery of visual responsiveness following cortical damage. Finally, we will provide an overview of how callosal projections dysfunction could contribute to pathologies such as neglect and occipital epilepsy. A particular focus will be on reviewing noninvasive brain stimulation techniques and optogenetic approaches that allow to selectively manipulate callosal function and to probe its involvement in cortical processing and plasticity. Overall, the data indicate that experience can potently impact on transcallosal connectivity, and that the callosum itself is crucial for plasticity and recovery in various disorders of the visual pathway.

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Environmental Enrichment Promotes Plasticity and Visual Acuity Recovery in Adult Monocular Amblyopic Rats

Cited by 39 publications

References 29 publications

Inhibitory Neuron Transplantation into Adult Visual Cortex Creates a New Critical Period that Rescues Impaired Vision

Inhibitory Neuron Transplantation into Adult Visual Cortex Creates a New Critical Period that Rescues Impaired Vision

Consequences of brain-derived neurotrophic factor withdrawal in CNS neurons and implications in disease

Reorganization of Visual Callosal Connections Following Alterations of Retinal Input and Brain Damage

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