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Article: Restoring visual function after photoreceptor degeneration: Ectopic expression of photosensitive proteins in retinal neurons

TitleRestoring visual function after photoreceptor degeneration: Ectopic expression of photosensitive proteins in retinal neurons
Authors
KeywordsAav
Bipolar Cells
Channelrhodopsin
Ganglion Cells
Gene Therapy
Melanopsin
Photoreceptor Degeneration
Issue Date2011
Citation
Neuromethods, 2011, v. 55, p. 147-164 How to Cite?
AbstractA leading cause of blindness worldwide is degeneration of the retinal photoreceptor cells. The two large classes of such disorders are retinitis pigmentosa, which affects ∼100,000 individuals in the USA, and macular degeneration, which affects ∼3,000,000. The causes of both disorders are diverse, but the initial lesion in both cases is to the rod and cone photoreceptor cells, leaving a retina in which many neurons appear functionally intact, but the retina - either the entire tissue or specific regions of it - can no longer detect light. A strategy for restoring at least a minimal level of vision is to engineer the expression of a photosensitive molecule in the surviving, nonphotoreceptor, neurons. This has been achieved at the level of proof of principle in the rd strain of mice, which undergoes photoreceptor degeneration similar to retinitis pigmentosa. In separate experiments, Channelrhodopsin-2 or melanopsin were introduced into retinal neurons and restoration of electrophysiological responsiveness and simple visually guided behaviors was demonstrated. There is reason for cautious optimism that vision aided in this way may eventually be of use for humans suffering from photoreceptor degenerations. © 2011 Humana Press.
Persistent Identifierhttp://hdl.handle.net/10722/149759
ISSN
2015 SCImago Journal Rankings: 0.173
References

 

DC FieldValueLanguage
dc.contributor.authorLin, Ben_US
dc.contributor.authorMasland, RHen_US
dc.date.accessioned2012-06-26T05:58:10Z-
dc.date.available2012-06-26T05:58:10Z-
dc.date.issued2011en_US
dc.identifier.citationNeuromethods, 2011, v. 55, p. 147-164en_US
dc.identifier.issn0893-2336en_US
dc.identifier.urihttp://hdl.handle.net/10722/149759-
dc.description.abstractA leading cause of blindness worldwide is degeneration of the retinal photoreceptor cells. The two large classes of such disorders are retinitis pigmentosa, which affects ∼100,000 individuals in the USA, and macular degeneration, which affects ∼3,000,000. The causes of both disorders are diverse, but the initial lesion in both cases is to the rod and cone photoreceptor cells, leaving a retina in which many neurons appear functionally intact, but the retina - either the entire tissue or specific regions of it - can no longer detect light. A strategy for restoring at least a minimal level of vision is to engineer the expression of a photosensitive molecule in the surviving, nonphotoreceptor, neurons. This has been achieved at the level of proof of principle in the rd strain of mice, which undergoes photoreceptor degeneration similar to retinitis pigmentosa. In separate experiments, Channelrhodopsin-2 or melanopsin were introduced into retinal neurons and restoration of electrophysiological responsiveness and simple visually guided behaviors was demonstrated. There is reason for cautious optimism that vision aided in this way may eventually be of use for humans suffering from photoreceptor degenerations. © 2011 Humana Press.en_US
dc.languageengen_US
dc.relation.ispartofNeuromethodsen_US
dc.subjectAaven_US
dc.subjectBipolar Cellsen_US
dc.subjectChannelrhodopsinen_US
dc.subjectGanglion Cellsen_US
dc.subjectGene Therapyen_US
dc.subjectMelanopsinen_US
dc.subjectPhotoreceptor Degenerationen_US
dc.titleRestoring visual function after photoreceptor degeneration: Ectopic expression of photosensitive proteins in retinal neuronsen_US
dc.typeArticleen_US
dc.identifier.emailLin, B:blin@hku.hken_US
dc.identifier.authorityLin, B=rp01356en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/978-1-61779-031-7_8en_US
dc.identifier.scopuseid_2-s2.0-79952405725en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79952405725&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume55en_US
dc.identifier.spage147en_US
dc.identifier.epage164en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLin, B=36165916900en_US
dc.identifier.scopusauthoridMasland, RH=7007167900en_US

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