Brief Communication Retinogeniculate Axons Undergo Eye-Specific Segregation in the Absence.pdf

Brief Communication Retinogeniculate Axons Undergo Eye-Specific Segregation in the Absence of Eye-Specific Layers Gianna Muir-Robinson,1 Bryan J. Hwang,2 and Marla B. Feller1 1Neurobiology Section, Biology Division, University of California San Diego, La Jolla, California 92093, and 2Howard Hughes Medical Institute–National Institutes of Health Research Scholars Program, Bethesda, Maryland 20892 Spontaneous retinal activity mediated by cholinergic transmission regulates the segregation of retinal ganglion cell axons in the lateral geniculate nucleus of the thalamus into eye-specific layers. The details of how the layers form are unknown. Mice lacking the
2 subunit of the neuronal nicotinic acetylcholine receptor lack ACh-mediated waves and as a result, do not form eye-specific layers at any stage of development. However, during the second postnatal week,
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mice have glutamate-mediated waves. Here we show that after the first postnatal week, even in the absence of layers, retinothalamic axons segregate into an unlay- ered, patchy distribution of eye-specific regions. These results indicate that spontaneous neural activity may independently reg- ulate eye-specific segregation and the formation of layers at the developing retinothalamic projection. Key words: retinogeniculate segregation; retinal waves; spon- taneous activity; visual-system development; eye-specific lay- ers; nicotinic receptor subunits The development of precise neural circuitry involves activity- dependent refinement of an initially crude set of connections. This process has been studied extensively in the visual system of binocular animals, where retinal ganglion cell axons from the two eyes organize into eye-specific layers in the lateral geniculate nucleus (LGN). These layers are examples of macroscopic struc- tures reflecting bulk organization of thousands of axons on the millimeter-length scale in ferrets and cats and the hundreds of micron-length scale in mice. The proposed mechanisms unde