Network influences on cortical plasticity

Greifzu, Franziska; Wolf, Fred; Löwel, Siegrid

doi:10.1007/s13295-012-0030-0

Cited by 6 publications

(4 citation statements)

References 40 publications

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“…These changes include both functional as well as structural modifications and are considered to be fundamental for development (Berardi et al, 2015). Moreover, it was shown that while plastic changes may be well circumscribed, they still have repercussions in other areas of the CNS, distant or contiguous (Greifzu et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Neural plasticity and network remodeling: From concepts to pathology

et al. 2017

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Section: Introductionmentioning

confidence: 99%

Neural plasticity and network remodeling: From concepts to pathology

et al. 2017

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“…In V1 of C57Bl/6J mice, this OD-plasticity is maximal at 4 weeks of age, declines in 2-3 month old animals and is absent beyond PD110 (Espinosa and Stryker, 2012;Levelt and Hübener, 2012), even after longer deprivation times (Greifzu et al, 2012), if animals are raised in standard cages (SC). In critical period mice (PD19-32), 4 days of MD are sufficient to induce OD-shifts towards the open eye (Gordon and Stryker, 1996).…”

Section: Introductionmentioning

confidence: 99%

Brief dark exposure restored ocular dominance plasticity in aging mice and after a cortical stroke

Stodieck

Greifzu

Goetze

et al. 2014

Experimental Gerontology

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In the primary visual cortex (V1), monocular deprivation (MD) induces a shift in the ocular dominance (OD) of binocular neurons towards the open eye (Wiesel and Hubel, 1963; Gordon and Stryker, 1996). In V1 of C57Bl/6J mice, this OD-plasticity is maximal in juveniles, declines in adults and is absent beyond postnatal day (PD) 110 (Lehmann and Löwel, 2008) if mice are raised in standard cages. Since it was recently shown that brief dark exposure (DE) restored OD-plasticity in young adult rats (PD70-100) (He et al., 2006), we wondered whether DE would restore OD-plasticity also in adult and old mice and after a cortical stroke. To this end, we raised mice in standard cages until adulthood and transferred them to a darkroom for 10-14 days. Using intrinsic signal optical imaging we demonstrate that short-term DE can restore OD-plasticity after MD in both adult (PD138) and old mice (PD535), and that OD-shifts were mediated by an increase of open eye responses in V1. Interestingly, restored OD-plasticity after DE was accompanied by a reduction of both parvalbumin expressing cells and perineuronal nets and was prevented by increasing intracortical inhibition with diazepam. DE also maintained OD-plasticity in adult mice (PD150) after a stroke in the primary somatosensory cortex. In contrast, short-term DE did not affect basic visual parameters as measured by optomotry. In conclusion, short-term DE was able to restore OD-plasticity in both adult and aging mice and even preserved plasticity after a cortical stroke, most likely mediated by reducing intracortical inhibition.

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“…While the binocular part of V1 receives input from both eyes, the monocular part of V1 receives input from the contralateral eye only. Figure modified from Greifzu et al (2012).…”

Section: Visual System and Od-plasticitymentioning

confidence: 99%

Enhancing visual cortical plasticity in mice by enriching their environment: a combined imaging and behavioural study

Kalogeraki¹

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Brain plasticity is important not only for normal brain functions like learning and memory, but is also crucial for recovery after injuries. It has been shown that the environment has a great influence on brain plasticity. Here, I investigate the impact of an enriched environment (EE) on ocular dominance (OD) plasticity of the mouse primary visual cortex (V1), using monocular deprivation (MD) as a model to trigger OD-plasticity and optical imaging of intrinsic signals to monitor it. Additionally, a variety of behavioural tests was used to measure the visual abilities of mice and their alteration after MD. OD-plasticity in V1 is an agedepended phenomenon: it is maximal during the critical period (postnatal day (PD) 21-35), reduced but still present in young adult mice (2-3 months) and absent in fully mature animals (beyond PD110). This age dependence holds true for mice raised in standard cages (SC), however we showed that raising mice in a more complex environment could not only prolong the sensitive phase for OD-plasticity into adulthood but also reinduce OD-plasticity in mice transferred to EE after PD110. Interestingly, the observed OD-plasticity in old EE-mice was similar to that in SC-mice during the critical period, suggesting that EE-housing resulted in a more juvenile brain. Additionally, we found that EE-raising can enable even lifelong ODplasticity (up to PD900). Using behavioural tests we also showed that EE-raising did not affect the visual abilities of old mice and did not increase the interindividual variability. To test whether OD-plasticity in adult EE-mice is indeed juvenile-like, we tested different age groups of EE-mice after 4 days of MD. We found that 4 days of MD can induce an OD-shift in all the age groups of EE-mice tested, but the OD-shift in young and fully mature EE-mice was similar to adult OD-plasticity observed in around 3 month old SC-mice.EE-raising provides mice with increased social interactions, physical exercise and cognitive stimulation compared to SC rearing. We asked the question, whether all components are needed or just one of them is already sufficient to prolong OD-plasticity. We tested whether voluntary physical exercise alone prolongs OD-plasticity by raising mice in SCs equipped with a running wheel (RW). RW-raised mice continued to show an OD-plasticity into adulthood, while mice without a RW did not. Moreover, running only for 7 days was sufficient to restored OD-plasticity in adult SC-raised mice. In addition, the OD-shift of RWmice was mediated by a decrease in deprived eye responses, which was previously seen only in critical period SC-mice or in adult EE-mice.It was previously shown, that a small lesion in the primary somatosensory cortex (S1) prevented both cortical plasticity and improvement of visual abilities in the adult mouse visual system after MD. However, in adult EE-mice, OD-plasticity was preserved after stroke induction and the improvement of visual abilities was partially preserved. Here, we investigated, whether raising mice in a cage with a RW wil...

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Network influences on cortical plasticity

Cited by 6 publications

References 40 publications

Neural plasticity and network remodeling: From concepts to pathology

Neural plasticity and network remodeling: From concepts to pathology

Brief dark exposure restored ocular dominance plasticity in aging mice and after a cortical stroke

Enhancing visual cortical plasticity in mice by enriching their environment: a combined imaging and behavioural study

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