Retinal waves in mice lacking the beta2 subunit of the nicotinic acetylcholine receptor.

Proc Natl Acad Sci U S A

Departments of Neurobiology, Physiology, and Behavior, and Ophthalmology and Vision Science, University of California, Davis, CA 95616, USA.

Published: September 2008

AI Article Synopsis

  • The beta2 subunit of the nicotinic acetylcholine receptor is crucial for normal development in the visual system, as seen in mutant animals lacking this subunit.
  • These mutants show abnormal eye-specific retinogeniculate projections, often attributed to a lack of correlated activity in developing retinas.
  • However, recent findings reveal that these mutants do have robust retinal waves, but they are transmitted differently than in normal animals, suggesting that other factors beyond retinal waves contribute to visual system deficits in these mutants.

Article Abstract

The structural and functional properties of the visual system are disrupted in mutant animals lacking the beta2 subunit of the nicotinic acetylcholine receptor. In particular, eye-specific retinogeniculate projections do not develop normally in these mutants. It is widely thought that the developing retinas of beta2(-/-) mutants do not manifest correlated activity, leading to the notion that retinal waves play an instructional role in the formation of eye-specific retinogeniculate projections. By multielectrode array recordings, we show here that the beta2(-/-) mutants have robust retinal waves during the formation of eye-specific projections. Unlike in WT animals, however, the mutant retinal waves are propagated by gap junctions rather than cholinergic circuitry. These results indicate that lack of retinal waves cannot account for the abnormalities that have been documented in the retinogeniculate pathway of the beta2(-/-) mutants and suggest that other factors must contribute to the deficits in the visual system that have been noted in these animals.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2527347PMC
http://dx.doi.org/10.1073/pnas.0807178105DOI Listing

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