Probing inner retinal circuits in the rod pathway: a comparison of c-fos activation in mutant mice

Vis Neurosci. Nov-Dec 2004;21(6):873-81. doi: 10.1017/S0952523804216078.

Abstract

We have used wild-type mice and mice possessing defects in specific retinal circuits in order to more clearly define functional circuits of the inner retina. The retina of the nob mouse lacks communication between photoreceptors and depolarizing bipolar cells (DBCs). Thus, all light driven activity in the nob mouse is mediated via remaining hyperpolarizing bipolar cell (HBC) circuits. Transducin null (Tr alpha-/-) mice lack rod photoreceptor activity and thus remaining retinal circuits are solely generated via cone photoreceptor activity. Activation in inner retinal circuits in each of these mice was identified by monitoring light-induced expression of an immediate early gene, c-fos. The number of cells expressing c-fos in the inner retina was dependent upon stimulus intensity and was altered in a systematic fashion in mice with known retinal mutations. To determine whether c-fos is activated via circuits other than photoreceptors in the outer retina, we examined c-fos expression in tulp1-/- mice that lack photoreceptors in the outer retina; these mice showed virtually no c-fos activity following light exposure. Double-labeling immunohistochemical studies were carried out to more clearly define the population of c-fos expressing amacrine cells. Our results indicate that c-fos may be used to map functional circuits in the retina.

Publication types

  • Comparative Study
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Electroretinography
  • Eye Proteins / genetics
  • Immunohistochemistry
  • Light
  • Mice
  • Mice, Knockout / genetics
  • Photoreceptor Cells, Vertebrate / physiology
  • Proto-Oncogene Proteins c-fos / metabolism*
  • Retina / metabolism
  • Retina / physiology*
  • Retina / radiation effects
  • Retinal Cone Photoreceptor Cells / physiology
  • Retinal Rod Photoreceptor Cells / physiology*
  • Transducin / deficiency
  • Transducin / genetics
  • Visual Pathways / metabolism
  • Visual Pathways / physiology*

Substances

  • Eye Proteins
  • Proto-Oncogene Proteins c-fos
  • Tulp1 protein, mouse
  • Transducin