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Laminin deficits induce alterations in the development of dopaminergic neurons in the mouse retina

Published online by Cambridge University Press:  22 August 2007

VIKTÓRIA DÉNES
Affiliation:
Department of Anatomy and Cellular Biology, Tufts University School of Medicine, Boston, Massachusetts Tufts Center for Vision Research, Boston, Massachusetts
PAUL WITKOVSKY
Affiliation:
Department of Ophthalmology, New York University School of Medicine, New York, New York
MANUEL KOCH
Affiliation:
Center for Biochemistry and Department of Dermatology, University of Köln, Köln, Germany
DALE D. HUNTER
Affiliation:
Tufts Center for Vision Research, Boston, Massachusetts
GERMÁN PINZÓN-DUARTE
Affiliation:
Department of Anatomy and Cellular Biology, Tufts University School of Medicine, Boston, Massachusetts Tufts Center for Vision Research, Boston, Massachusetts
WILLIAM J. BRUNKEN
Affiliation:
Department of Anatomy and Cellular Biology, Tufts University School of Medicine, Boston, Massachusetts Tufts Center for Vision Research, Boston, Massachusetts

Abstract

Genetically modified mice lacking the β2 laminin chain (β2null), the γ3 laminin chain (γ3 null), or both β2/γ3 chains (compound null) were produced. The development of tyrosine hydroxylase (TH) immunoreactive neurons in these mouse lines was studied between birth and postnatal day (P) 20. Compared to wild type mice, no alterations were seen in γ3 null mice. In β2 null mice, however, the large, type I TH neurons appeared later in development, were at a lower density and had reduced TH immunoreactivity, although TH process number and size were not altered. In the compound null mouse, the same changes were observed together with reduced TH process outgrowth. Surprisingly, in the smaller, type II TH neurons, TH immunoreactivity was increased in laminin-deficient compared to wild type mice. Other retinal defects we observed were a patchy disruption of the inner limiting retinal basement membrane and a disoriented growth of Müller glial cells. Starburst and AII type amacrine cells were not apparently altered in laminin-deficient relative to wild type mice. We postulate that laminin-dependent developmental signals are conveyed to TH amacrine neurons through intermediate cell types, perhaps the Müller glial cell and/or the retinal ganglion cell.

Type
Research Article
Copyright
© 2007 Cambridge University Press

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