Abstract
The rate-limiting step in the recovery of the photoreceptor light response is the hydrolysis of GTP by transducin, a reaction that is accelerated by the RGS9-Gβ5 complex, and its membrane anchor, R9AP. Similar complexes, including RGS7, RGS11, and Gβ5, are found in retinal ON-bipolar cell dendrites. Here, we present evidence that R9AP is also expressed in the dendritic tips of ON-bipolar cells. Immunofluorescent staining for R9AP revealed a punctate pattern of labeling in the outer plexiform layer, where it colocalized with mGluR6. In photoreceptors, R9AP is required for proteolytic stability of the entire regulator of G protein signaling complex, and we found that genetic deletion of R9AP also results in a marked reduction in the levels of RGS11 and Gβ5 in the bipolar cell dendrites; the level of RGS7 was unaffected, suggesting the presence of another interaction partner to stabilize RGS7. To determine the effect of R9AP deletion on the response kinetics of ON-bipolar cells, we compared the electroretinogram (ERG) between wild-type and R9AP-deficient mice. The ERG b-wave, reflecting ON-bipolar cell activity, was delayed and larger in the R9AP-deficient mice. Our data indicate that R9AP is required for stable expression of RGS11-Gβ5 in ON-bipolar cell dendrites. Furthermore, they suggest that the RGS11-Gβ5-R9AP complex accelerates the initial ON-bipolar cell response to light.
Original language | English (US) |
---|---|
Pages (from-to) | 9-17 |
Number of pages | 9 |
Journal | Visual neuroscience |
Volume | 27 |
Issue number | 1-2 |
DOIs | |
State | Published - Mar 2010 |
Keywords
- ERG b-wave
- Electroretinogram
- RGS proteins
- Retina
ASJC Scopus subject areas
- Physiology
- Sensory Systems