Bryan William Jones, Ph.D. Moran Eye Center Salt Lake City, Utah https://marclab.org
Friday, October 24, 2014 3:00 – 4:00 p.m.
Cancer Research Building Auditorium
In normal retina, free from degenerative disease or trauma, retinal photoreceptors drive signal processing networks in neural retina comprising bipolar, horizontal, amacrine and ganglion cells. Conventional wisdom held that retinal degenerative diseases such as retinitis pigmentosa (RP) affect only sensory retina, leaving neural retina relatively unscathed. This is unfortunately, still commonly believed, but incorrect as the resulting loss of rod and cone input to the neural retina constitutes differentiation and remodeling at the cellular and molecular level becomes unavoidable.
RP is a collection of progressive pathologies with defects at molecular, cellular and tissue levels in natural and engineered models of retinal degeneration. Though it should be noted that retinal degenerations can result from retinal detachment, AMD or any other situation where photoreceptors are lost, particularly cones. Photoreceptor loss effectively deafferents the neural retina, triggering a series of phased plastic revisions to the neural retina called retinal remodeling. This talk will address the phased revision of the adult retina in response to differentiation, encompassing subsequent retinal plasticity with revisions to neuronal morphology and topology through neurogenesis, cell migration, gene expression, protein expression, glutamate channel function, synaptic and likely gap-junctional connectivities.