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Laminin modulates neuritogenesis of developing rat retinal ganglion cells through a protein kinase C‐dependent pathway
Author(s) -
de AryPires Ricardo,
Linden Rafael
Publication year - 2000
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(20000501)60:3<291::aid-jnr3>3.0.co;2-y
Subject(s) - forskolin , protein kinase c , microbiology and biotechnology , laminin , brain derived neurotrophic factor , neurotrophic factors , protein kinase a , biology , retina , chemistry , kinase , neuroscience , biochemistry , receptor , extracellular matrix
Dissociated cells from rat retinae (P2–P21) were cultured to investigate interactions between brain‐derived neurotrophic factor (BDNF), various substrates (poly‐L‐lysine, collagen, and laminin), and protein kinases upon the neuritogenesis of retinal ganglion cells (RGCs). We found that BDNF‐promoted neuritogenesis was enhanced by forskolin in RGCs from rats at P2–P21 plated on either poly‐L‐lysine or collagen. In contrast, in cultures with a laminin substrate, the enhancer effect of forskolin was observed only in RGCs taken from the retina of rats at P2–P6. Laminin blocked the enhancement of BDNF‐induced RGCs neuritogenesis by forskolin, in RGCs from either P14 or P21, and induced a tenfold increase of protein kinase C (PKC) activity compared to poly‐L‐lysine. This blockade was reverted with a selective PKC inhibitor and was reproduced in poly‐L‐lysine cultures of P14–P21 RGCs with a PKC activator. Because axotomized RGCs need both BDNF and forskolin to regenerate, we suggest that laminin can hinder this effect by simultaneous PKC activation according to a developmentally regulated pattern. We further propose a model of interaction in the optic pathways triggered by BDNF, forskolin, and laminin that may be useful in elucidating some of the biological effects seen with regenerating axons. J. Neurosci. Res. 3:291–301, 2000 © 2000 Wiley‐Liss, Inc.