Environmental enrichment in adulthood promotes amblyopia recovery through a reduction of intracortical inhibition

Sale, Alessandro; Maya‐Vetencourt, José Fernando; Medini, Paolo; Cenni, Maria Cristina; Baroncelli, Laura; Pasquale, Roberto De; Maffei, Lamberto

doi:10.1038/nn1899

Cited by 430 publications

(492 citation statements)

References 14 publications

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“…Our results are quite similar to those obtained with other protocols, including environmental enrichment, both at the level of functional reactivation of plasticity in adulthood 30,32 and at the level of increase in histone acetylation 44 . In spite of this, some of the molecular mechanisms associated with recovery of plasticity in environmental enrichment and FR seem to be different.…”

Section: Discussionsupporting

confidence: 89%

“…In the last few years, the excitation-inhibition balance in the brain has been increasingly recognized as a crucial hub for the restoration of plasticity in the adult nervous system 39 . It has been demonstrated that the pharmacological or physiological reduction of inhibition in the visual cortex of adult rats is sufficient to restore OD shift in response to MD 23,[30][31][32] . Here, we show that FR is associated with a marked reduction of GABAergic inhibition, as evaluated using both biochemical and electrophysiological methods, and we also provide evidence that an artificial increase of inhibition in the visual cortex by infusion of the benzodiazepine diazepam prevents the OD shift due to MD in FR rats.…”

Section: Discussionmentioning

confidence: 99%

“…Restoration of plasticity in the adult has been often associated with increased levels of neurotrophins and remodelling of extracellular matrix [29][30][31][32] . We tested whether FR affected brain-derived neurotrophic factor (BDNF) content in the adult visual cortex by means of immunohistochemistry and western blot.…”

Section: Corticosterone Mimics Fr Effects On Visual Cortex Plasticitymentioning

confidence: 99%

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Food restriction enhances visual cortex plasticity in adulthood

Spolidoro¹,

Baroncelli²,

Putignano

et al. 2011

Nat Commun

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neural circuits display a heightened sensitivity to external stimuli during well-established windows in early postnatal life. After the end of these critical periods, brain plasticity dramatically wanes. The visual system is one of the paradigmatic models for studying experiencedependent plasticity. Here we show that food restriction can be used as a strategy to restore plasticity in the adult visual cortex of rats. A short period of food restriction in adulthood is able both to reinstate ocular dominance plasticity and promote recovery from amblyopia. These effects are accompanied by a reduction of intracortical inhibition without modulation of brainderived neurotrophic factor expression or extracellular matrix structure. our results suggest that food restriction could be investigated as a potential way of modulating plasticity.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Section: Corticosterone Mimics Fr Effects On Visual Cortex Plasticitymentioning

confidence: 99%

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Food restriction enhances visual cortex plasticity in adulthood

Spolidoro¹,

Baroncelli²,

Putignano

et al. 2011

Nat Commun

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“…This suggests that the search for therapeutic strategies for these deficiencies should include strategies that increase TrkB/BDNF signaling in the visual cortex. Indeed, antidepressants 12 and environmental enrichment 11,49 both lead to an increase in BDNF signaling in the rodent cortex and positively affect visual acuity. It will be interesting to examine the effects of environmental enrichment or antidepressant treatment on visual acuity in an aged population.…”

Section: Normalization Model Reliably Matches Experimental Datamentioning

confidence: 99%

“…BDNF mRNA and protein levels 8,9 and acuity 10 in the primary visual cortex (V1) responding to a monocularly deprived eye are all below normal. In amblyopic rats receiving environmental enrichment 11 or antidepressant treatment 12 , increased BDNF expression in the cortex was seen in parallel to the restoration of visual acuity. Moreover, transgenic mice overexpressing BDNF in the forebrain show a faster rise of cortical acuity 6 even when reared in darkness 13 .…”

mentioning

confidence: 95%

Contrast gain control and cortical TrkB signaling shape visual acuity

Heimel¹,

Saiepour²,

Chakravarthy³

et al. 2010

Nat Neurosci

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2The limits of visual acuity and contrast sensitivity are set by the eye, but what we perceive is determined by the visual cortex 1 . In healthy, mature people and animals, the visual acuities of the retina and the cortex are well-matched 2 , but this match is neither automatic nor unbreakable. Differences between cortical and retinal acuity are most apparent during development, when cortical acuity continues to rise after retinal development is completed 3 , and during aging, when behavioral acuity falls even without obvious changes in the eye or the thalamus 4 . Differences also occur as a result of cortical injury or erroneous development. This is the case with amblyopia, the most prevalent (2-4%) visual impairment in young people. Amblyopia is a reduced psychophysical acuity in one or both eyes. It is believed to be caused by deficient processing in the visual cortex 5 , but the mechanisms underlying the dissociations of retinal and cortical acuity in amblyopia and in the healthy aging and developing brain are unclear. Interestingly, there is a good match between changes in the cortical expression level of brain-derived neurotrophic factor (BDNF) and changes in visual acuity.During development, acuity and BDNF levels rise 6 , while both slowly decrease with age 4,7 . This relationship between BDNF and acuity also holds for experimentally induced amblyopia. BDNF mRNA and protein levels 8,9 and acuity 10 in the primary visual cortex (V1) responding to a monocularly deprived eye are all below normal. In amblyopic rats receiving environmental enrichment 11 or antidepressant treatment 12 , increased BDNF expression in the cortex was seen in parallel to the restoration of visual acuity. Moreover, transgenic mice overexpressing BDNF in the forebrain show a faster rise of cortical acuity 6 even when reared in darkness 13 . Although there is a wealth of data on the involvement of BDNF and its main receptor TrkB in neuronal development 14 , synaptic efficacy 15 , -morphology 16 and -plasticity 17,18 , it has remained unknown how BDNF promotes visual acuity at the coding level and whether BDNF signaling plays a role in acuity in the mature cortex. For these reasons we studied visual acuity in adult transgenic mice where, after normal development is completed, cortical TrkB/BDNF signaling is impaired. We found a loss of acuity, caused by a reduction in apparent contrast. Using a combination of experiments and modeling, we show the involvement of cortical gain control in the selective loss of responses to visual stimuli with high spatial frequencies and the maintenance of responses to low spatial frequencies. RESULTS Genetic inhibition of TrkB signaling in the adult cortexTo investigate the role of TrkB signaling in cortical acuity in the mature animal we overexpressed a dominant negative TrkB.T1-EGFP fusion protein 19 in a large proportion of pyramidal cells after the maturation of cortical acuity. This was achieved by crossing mice carrying a Cre-dependent TrkB.T1-EGFP-transgene under the control of the Thy-1 promoter ...

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Neuronal Network Plasticity and Recovery From Depression

2013

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The brain processes sensory information in neuronal networks that are shaped by experience, particularly during early life, to optimally represent the internal and external milieu. Recent surprising findings have revealed that antidepressant drugs reactivate a window of juvenile-like plasticity in the adult cortex. When antidepressant-induced plasticity was combined with appropriate rehabilitation, it brought about a functional recovery of abnormally wired neuronal networks. These observations suggest that antidepressants act permissively to facilitate environmental influence on neuronal network reorganization and so provide a plausible neurobiological explanation for the enhanced effect of combining antidepressant treatment with psychotherapy. The results emphasize that pharmacological and psychological treatments of mood disorders are closely entwined: The effect of antidepressant-induced plasticity is facilitated by rehabilitation, such as psychotherapy, that guides the plastic networks, and psychotherapy benefits from the enhanced plasticity provided by the drug treatment. Optimized combinations of pharmacological and psychological treatments might help make best use of existing antidepressant drugs and reduce the number of treatment-resistant patients. The network hypothesis of antidepressant action presented here proposes that recovery from depression and related mood disorders is a gradual process that develops slowly and is facilitated by structured guidance and rehabilitation.

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Environmental enrichment in adulthood promotes amblyopia recovery through a reduction of intracortical inhibition

Cited by 430 publications

References 14 publications

Food restriction enhances visual cortex plasticity in adulthood

Food restriction enhances visual cortex plasticity in adulthood

Contrast gain control and cortical TrkB signaling shape visual acuity

Neuronal Network Plasticity and Recovery From Depression

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