Abstract
The visual cortex is organized into retinotopic maps that preserve an orderly representation of the visual world, achieved by topographically precise inputs from the lateral geniculate nucleus. We show here that geniculocortical mapping is imprecise when the waves of spontaneous activity in the retina during the first postnatal week are disrupted genetically. This anatomical mapping defect is present by postnatal day 8 and has functional consequences, as revealed by optical imaging and microelectrode recording in adults. Pharmacological disruption of these retinal waves during the first week phenocopies the mapping defect, confirming both the site and the timing of the disruption in neural activity responsible for the defect. Analysis shows that the geniculocortical miswiring is not a trivial or necessary consequence of the retinogeniculate defect. Our findings demonstrate that disrupting early spontaneous activity in the eye alters thalamic connections to the cortex.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 797-809 |
| Number of pages | 13 |
| Journal | Neuron |
| Volume | 48 |
| Issue number | 5 |
| DOIs | |
| State | Published - Dec 8 2005 |
Funding
We thank Dr. Art Beaudet, for making this study possible by providing heterozygous β2 mice and Dr. Marla Feller, for providing homozygous β2 mice for our pilot experiments and for comments on the manuscript. We also thank Liz Hawkes, for genotyping; Ann Schreiber, for sectioning; and Drs. David Feldheim, Patrick McQuillen, Andrew Huberman, Andrew Tan, and members of the Stryker lab, for discussions. Our work is supported by N.I.H. grants to M.P.S. and D.R.C. J.C. is an Aventis Pharmaceuticals Fellow of the Life Sciences Research Foundation. Additional support was provided by That Man May See, Research to Prevent Blindness, and the Knights Templar Eye Foundation.
ASJC Scopus subject areas
- General Neuroscience