Astrocytes are now being acknowledged as major production sites for a large variety of cytokines serving the maintenance of neurons, renewal of glial cells, and orchestration of lesion responses. Understanding mechanisms that underlay the regulation of expression of growth factors derived from astrocytes is essential for designing novel therapeutic strategies in neurodegenerative disorders including Parkinson's disease (PD), M. Alzheimer, and ALS. A general aspect of growth factor functions in the brain is their contextuality. Taking studies related to cytokine-mediated astroglial cell proliferation as an example it becomes clear that one factor can inhibit or stimulate cell division depending on the presence or absence of other cytokines. This has an impact on in vitro experiments, which will have to analyze in much greater detail than hitherto done growth factor interactions and interdependencies. This presentation reviews studies of our laboratory on three growth factor families, CNTF, FGF, and TGF-[beta ]s Their effects and regulation in astroglial cells are of particular interest from a clinical point of view, since all of them have been shown to possess prominent trophic and protective activities for lesioned CNS neurons.CNTF: This factor is expressed at low levels in the adult brain, and most types of lesions and pharmological treatments of cultured astrocytes down-regulate expression of this important neurotrophic factor. CNTF itself, however, can upregulate its own expression in semi-confluent astroglial cell cultures.FGF: Several members of the FGF family including FGF-1, 2, -5, -8, and -9 are expressed in the brain. Functions related to neural cells include stimulation of astroglial cell proliferation, plasminogen activator, induction of neurotrophic molecules including NGF, and trophic functions for most CNS neuron populations. FGF-2 administered to cultured nigrostriatal dopaminergic neurons and animal models of PD has pronounced neuroprotective and restorative effects. Astroglial cells seem to be involved in mediating neurotrophic effects of FGF both in vitro and in vivo, possibly by increasing their expression of trophically acting cytokines.TGF-[beta ]s: This superfamily of multifunctional cytokines is widely represented in the developing and/or adult CNS. TGF0[beta ]1-3 participate in the regulation of astroglial proliferation, maturation, and gene expression. Moreover, TGF-[beta ]s including the distantly related GDNF promote survival of developing and toxically impaired nigrostriatal neurons and may become relevant for novel therapies in PD. GDNF expression can be upregulated in C6 glioma cells. Levels of GDNF in astroglial cells cultured from neonatal rat cortices and within the adult brain, however, are very low or undectable suggesting that it will be difficult to develop strategies for raising GDNF concentrations in the CNS by pharmacological interventions.