Laminin modulates neuritogenesis of developing rat retinal ganglion cells through a protein kinase C-dependent pathway
✍ Scribed by Ricardo de Ary-Pires; Rafael Linden
- Publisher
- John Wiley and Sons
- Year
- 2000
- Tongue
- English
- Weight
- 210 KB
- Volume
- 60
- Category
- Article
- ISSN
- 0360-4012
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✦ Synopsis
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 BDNFinduced 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-Llysine. 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.