Glial cells, lead-induced

Fig,1, Dual effect of cannabinoids on the viability oftransformed versus non-transformed glial cells. In glioma cells, cannabinoids activate CBq and CB2 receptors, inducing sustained ceramide accumulation and inhibition ofthe pro-survival kinase Akt, leading in turn to apoptosis. In normal astrocytes, cannabinoids activate CBi receptors, preventing ceramide-induced Akt inhibition and leading in turn to cell survival... 

The mechanisms underlying the mitogenic response of glial cells to FGF have been studied in some detail not surprisingly, activation of tyrosine kinase activity, followed by activation of phospholipase C and protein kinase C and leading to increased c-fos expression, are key initial steps (Radhakrishna and Almazan, 1994). In 02-A progenitor cells, FGF-2 has been shown to induce the... 

Chronic low-level lead exposure has been demonstrated to inhibit neural cell acquisition and impair early postnatal structuring of the central nervous system. Lead was demonstrated to have an anti-mitotic action both in vitro and in vivo, although the latter was confined to the cerebellum at blood lead threshold values of 30-40 jUg/dl. Low-level lead exposure more potently affected in vivo cell positioning and fibre outgrowth, as judged by the impaired developmental desialylation of the D2-CAM/N-CAM protein, and these effects were seen at blood lead threshold values of 20-30 jUg/dl. This inhibition of normal D2-CAM/N-CAM desialylation is attributed to improper guidance of neuronal cells and their fibres, as lead is demonstrated to specifically induce precocious differentiation of the glial cells. 

Lead-induced differentiation of glial cells in vitro and in vivo... 

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