| First Author | Yang RB | Year | 1999 |
| Journal | J Neurosci | Volume | 19 |
| Issue | 14 | Pages | 5889-97 |
| PubMed ID | 10407028 | Mgi Jnum | J:77627 |
| Mgi Id | MGI:2182189 | Doi | 10.1523/JNEUROSCI.19-14-05889.1999 |
| Citation | Yang RB, et al. (1999) Disruption of a retinal guanylyl cyclase gene leads to cone-specific dystrophy and paradoxical rod behavior. J Neurosci 19(14):5889-97 |
| abstractText | One of two orphan photoreceptor guanylyl cyclases that are highly conserved from fish to mammals, GC-E (or retGC1) was eliminated by gene disruption. Expression of the second retinal cyclase (GC-F) as well as the numbers and morphology of rods remained unchanged in GC-E null mice. However, rods isolated from such mice, despite having a normal dark current, recovered from a light flash markedly faster. Unexpectedly, the a- and b-waves of electroretinograms (ERG) from dark-adapted null mice were suppressed markedly. Cones, initially present in normal numbers in the retina, disappeared by 5 weeks, based on ERG and histology. Thus, the GC-E-deficient mouse defines a model for cone dystrophy, but it also demonstrates that morphologically normal rods display paradoxical behavior in their responses to light. |
