Reawakening plasticity in visual cortex

Thursday, October 21, 12:00 – 14:00 ET

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Recent advancements—ranging from molecular studies in animal models to behavioral studies in humans—have provided critical insights on the mechanisms governing the development of cortical function, and how they are influenced by environmental experience. Speakers in this session will focus on recent findings describing the cascade of events that controls the sensitive period, and discuss potential methods for remediating clinical conditions by selectively reopening plasticity.

This special session is being hosted by the Clinical Vision Sciences Technical Group along with the Fall Vision Meeting Planning Committee.

Invited Speakers:

  • Kevin Duffy, Dalhousie University

  • Takao Hensch, Harvard University

  • Claudia Lunghi, Laboratoire des Systèmes Perceptifs, Ecole Normale Supérieure

  • Elizabeth Quinlan, University of Maryland, College Park


  • Kimberly Meier, University of Washington

  • Ione Fine, University of Washington


Lifting brakes on visual cortical plasticity

Takao K. Hensch, Harvard University

Recovery from the effects of visual deprivation beyond peak plasticity

Kevin Duffy, Psychology & Neuroscience, Dalhousie University, Canada

Visual experience during early postnatal life plays an important role in the development of neural circuits that support normal vision. Conditions that disrupt visual experience can alter the structure and function of neurons to produce a functional impairment, amblyopia, in the affected eye that can last a lifetime. Susceptibility to the neural modifications presumed to underlie amblyopia is confined to the early years of life during the so-called critical period. Up until recently, recovery from the effects of visual deprivation was likewise thought to be possible only early life; however, research in rodents has demonstrated that under certain conditions recovery can occur at ages beyond the critical period. We have observed a remarkable recovery from the effects of visual deprivation in cats following temporary retinal inactivation with intraocular application of tetrodotoxin, a potent neural anesthetic. Notably, retinal inactivation produces rapid and significant structural and functional recovery at ages beyond what can be achieved with conventional therapy. This talk will present results from our studies on the use of retinal inactivation to resource plasticity capacity and promote recovery from the effects of early visual deprivation.

Funding Acknowledgement: Research funding provided by the Canadian Institutes of Health Research (CIHR) and the Natural Science and Engineering Research Council of Canada (NSERC).

Reactivating visual plasticity in adult humans

Claudia Lunghi, Laboratoire des Systèmes Perceptifs, Département d’Etudes Cognitives, Ecole Normale Supérieure, PSL University CNRS, Paris, France

Neuroplasticity is a fundamental property of the nervous system that is maximal early in life, within a specific temporal window called critical period. However, it is still unclear to which extent the plastic potential of the visual cortex is retained in adulthood. We have surprisingly revealed residual ocular dominance plasticity in adult humans by showing that short-term monocular deprivation unexpectedly boosts the deprived eye (both at the perceptual and at the neural level), reflecting homeostatic plasticity. This effect is accompanied by a decrease of GABAergic inhibition in the primary visual cortex and can be modulated by non-visual factors (physical exercise, motor plasticity and energy metabolism). Finally, we have found that combining short-term reverse occlusion with physical exercise promotes the long-term improvement in visual acuity and stereopsis in adult amblyopic patients. Taken together, these results challenge the classical view of a hard-wired adult visual cortex, indicating that homeostatic plasticity can be reactivated in adult humans.

Funding Acknowledgement: This project has received funding from the European Research Council (ERC, grant agreement No 948366 - HOPLA) and the French National Research Agency (ANR, grant agreement ANR-19-CE28-0008, PlaStiC).

Recovery from amblyopia in the adult mouse through dark exposure, light reintroduction and perisynaptic proteolysis

Elizabeth Quinlan, Department of Biology and Brain and Behavior Institute, University of Maryland, USA

An imbalance in the quality of visual input across the two eyes during development induces amblyopia, a disorder affecting up to 6% of the world’s population. In animal models, severe deprivation amblyopia can be induced by early-onset, chronic monocular occlusion, and is manifest as a loss of spatial acuity through the deprived eye and a decrease in the strength of neuronal responses evoked by deprived eye stimulation. In all species, amblyopia is highly resistant to reversal in adulthood, due in part to the decline in synaptic plasticity in the primary visual cortex with age. However, we have previously demonstrated that visual deprivation (dark exposure) followed by light reintroduction (LRx) rejuvenates plasticity in the adult amblyopic cortex. The reactivation of plasticity triggered by DE/LRx is mediated an increase in the activity of a matrix metalloproteinase (MMP9), that is perisynaptic, specific to thalamocortical synapses, and results in degradation of trans-synaptic adhesion proteins. Furthermore, live imaging of MMP activity in the mouse visual cortex demonstrates that DE lowers the threshold for MMP activation, enabling weak visual input through the amblyopic pathway to engage perisynaptic proteolysis. In amblyopic adult mice, the reactivation of synaptic plasticity by this novel and dynamic signaling pathway can be harnessed to promote full recovery of visually-evoked neuronal responses and spatial acuity.

Funding Acknowledgement: R01EY016431, R01EY025922.