Larkworthy Memorial Lecture: Reversing the effects of visual deprivation with retinal inactivation

Biography

He received his PhD from the Department of Psychology, Neuroscience & Behaviour at McMaster University under the supervision of Dr. Kathryn Murphy. His graduate research examined the influence that visual experience has on development of neurons within the primary visual pathway. As a post-doctoral fellow in the Department of Neurobiology at Harvard Medical School, he studied the structure and function of monkey visual cortex under the mentorship of Drs. Margaret Livingstone and David Hubel. Following post-doctoral training, he returned to Canada where he established his own laboratory at Dalhousie University. His research program investigates experience-dependent neural modifications that mediate perceptual impairments caused by abnormal vision. His lab has advanced understanding of the mechanisms that regulate neuroplasticity within the primary visual pathway, and has developed methods to manipulate plasticity through experiential interventions such as dark immersion and retinal inactivation. These approaches have demonstrated anatomical, physiological, and behavioral recovery from the effects of visual deprivation at developmental stages when conventional therapies typically show limited benefit.

Abstract

Visual experience in early postnatal life is critical for the development of neural circuits that support normal vision. Conditions that disrupt visual experience can alter the structure and function of neurons, producing a vision impairment called amblyopia that can last a lifetime. Recovery outcomes using mainstay therapies for amblyopia are limited by a number of factors that include poor patient compliance, prolonged treatment, and reduced efficacy beyond early childhood. In animal models, we have observed rapid recovery from the effects of monocular deprivation following temporary retinal inactivation of the dominant eye with intraocular application of tetrodotoxin, a potent neural anesthetic. Remarkably, retinal inactivation induced rapid and significant structural and functional recovery at ages beyond what is observed with conventional therapy. The recovery achieved with retinal inactivation occurred without apparent detriment to the inactivated eye. This talk will highlight results from our studies on the use of retinal inactivation to re-engage plasticity and promote recovery from the effects of early visual deprivation.