Block of gap junctions eliminates aberrant activity and restores light responses during retinal degeneration Academic Article uri icon

Overview

MeSH Major

  • Gap Junctions
  • Light Signal Transduction
  • Retinal Degeneration

abstract

  • Retinal degeneration leads to progressive photoreceptor cell death, resulting in vision loss. Subsequently, inner retinal neurons develop aberrant synaptic activity, compounding visual impairment. In retinal ganglion cells, light responses driven by surviving photoreceptors are obscured by elevated levels of aberrant spiking activity. Here, we demonstrate in rd10 mice that targeting disruptive neuronal circuitry with a gap junction antagonist can significantly reduce excessive spiking. This treatment increases the sensitivity of the degenerated retina to light stimuli driven by residual photoreceptors. Additionally, this enhances signal transmission from inner retinal neurons to ganglion cells, potentially allowing the retinal network to preserve the fidelity of signals either from prosthetic electronic devices, or from cells optogenetically modified to transduce light. Thus, targeting maladaptive changes to the retina allows for treatments to use existing neuronal tissue to restore light sensitivity, and to augment existing strategies to replace lost photoreceptors.

publication date

  • August 30, 2013

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC3756747

Digital Object Identifier (DOI)

  • 10.1523/JNEUROSCI.2399-13.2013

PubMed ID

  • 23986234

Additional Document Info

start page

  • 13972

end page

  • 7

volume

  • 33

number

  • 35