The Antidepressant Fluoxetine Restores Plasticity in the Adult Visual Cortex

Maya‐Vetencourt, José Fernando; Sale, Alessandro; Viegi, Alessandro; Baroncelli, Laura; Pasquale, Roberto De; O’Leary, Olivia F.; Ċastrén, Eero; Maffei, Lamberto

doi:10.1126/science.1150516

Cited by 806 publications

(857 citation statements)

References 26 publications

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“…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: Discussionmentioning

confidence: 99%

Section: Corticosterone Mimics Fr Effects On Visual Cortex Plasticitymentioning

confidence: 99%

Food restriction enhances visual cortex plasticity in adulthood

Spolidoro¹,

Baroncelli²,

Putignano

et al. 2011

Nat Commun

Self Cite

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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 .…”

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confidence: 96%

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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“…In mice injected with the MDA-MB213BR-GFP breast cancer cell line, Shapovalov et al [14] reported a 52% increase in total number of brain metastases in those mice that received fluoxetine in comparison to controls. These and an increase in plasticity [308,309]. In their brain metastasis model, Shapolvalov et al [14] found no association between PNN and fluoxetine.…”

Section: Current Research On Antidepressant Use and Cns Metastasismentioning

confidence: 98%