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 An eye opening look at adult visual plasticity
Article

An eye opening look at adult visual plasticity

 An eye opening look at adult visual plasticity
Article

An eye opening look at adult visual plasticity

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Transplantation of embryonic neurons reopens visual plasticity in adulthood


A new study from the Gandhi lab at the University of California, Irvine finds that transplantation of embryonic cortical interneurons into the adult visual cortex can reopen the critical period of plasticity in the visual system.


In juvenile mice, closure of one eye, or monocular deprivation, results in a permanent shift of visual responses from the closed eye to the open eye. This shift, called ocular dominance plasticity, only occurs during a critical period in development—in mice, at approximately 19 to 32 days old (P19-P32). In adult mice, the critical period is closed, or locked, and depriving one eye does not result in changed visual responses or plasticity.


In this study, Davis et al., transplanted embryonic neurons into adult mice to determine if the critical period could be unlocked later in life. Interneurons from the embryonic medial ganglionic eminence, which gives rise to inhibitory interneurons in the adult, were transplanted into the adult visual cortex. The transplanted embryonic interneurons migrated to their correct locations in the adult brain and made appropriate synaptic connections.


The authors also found that adult monocular deprivation—which normally has no effect on visual responses—when combined with transplantation of embryonic interneurons late in adulthood (long after the critical period), results in decreased visual responses from the deprived eye and increased visual responses from the preserved eye. This effectively unlocks the developmental period of visual plasticity. (The Gandhi lab and others have previously shown that transplanting embryonic interneurons into adult cortex shortly after the critical period can induce plasticity, but did not test this late in adulthood).1,2


Davis and colleagues then tested whether unlocking the critical period with interneuron transplantation rescues visual impairment caused by monocular deprivation during the juvenile critical period for visual plasticity. To do so, they deprived one eye from P19 to P32, then transplanted embryonic interneurons approximately 30 days after this period. Visual acuity and perception were measured 55 days later. Davis and colleagues found that visual acuity in the deprived eye recovered to levels found in the non-deprived eye after transplantation of embryonic interneurons.


The authors also determined that visual perception is restored in mice after transplantation: in a visual water task, untreated monocular deprivation resulted in impaired visual acuity in the deprived eye, while monocular deprivation followed later by transplantation of embryonic interneurons resulted in normal visual acuity in the deprived eye.


These results indicate that not only can transplantation of embryonic interneurons unlock the critical period for visual plasticity that is normally only present in early postnatal development, but that the induction of this plasticity can help restore lost visual function caused by lost visual input early in development. These data suggest that there may one day be new interventions for restoring visual perception later in life for children who have early vision deficits.


Publication

  1. Davis MF, Figueroa Velez DX, Guevarra RP, Yang MC, Habeeb M, Carathedathu MC, Gandhi SP (2015) Inhibitory Neuron Transplantation into Adult Visual Cortex Creates a New Critical Period that Rescues Impaired Vision. Neuron 86(4):1055–1066. doi: 10.1016/j.neuron.2015.03.062
References
  1. 1. Southwell DG, Froemke RC, Alvarez-Buylla A, Stryker MP, Gandhi SP (2010) Cortical plasticity induced by inhibitory neuron transplantation. Science 327(5969):1145–1148. doi: 10.1126/science.1183962
  2. 2. Tang Y, Stryker MP, Alvarez-Buylla A, Espinosa JS (2014) Cortical plasticity induced by transplantation of embryonic somatostatin or parvalbumin interneurons. Proceedings of the National Academy of Sciences 111(51):18339–18344. doi: 10.1073/pnas.1421844112
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