@article{SendtnerKreutzbergThoenen1990,
  author    = {Sendtner, Michael and Kreutzberg, Georg W. and Thoenen, Hans},
  title     = {Ciliary neurotrophic factor (CNTF) prevents the degeneration of motor neurons after axotomy},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-32637},
  year      = {1990},
  abstract  = {The period of natural cell death in the development of rodent motor neurons is followed by a period of sensitivity to axonal injury1-3. In the rat this early postnatal period of vulnerability coincides with that of very low ciliary neurotrophic factor (CNTF) levels in the sciatic nerve before CNTF increases to the high, adult levels4. The developmental time course of CNTF expression, its regional tissue distribution and its cytosolic localization (as suggested by its primary structure)4*5 favour a role for CNTF as a lesion factor rather than a target-derived neurotrophic molecule like nerve growth factor. Nevertheless CNTF exhibits neurotrophic activity in vitro on different populations of embryonic neurons6. To determine whether the vulnerability of motor neurons to axotomy in the early postnatal phase is due to insufficient availability of CNTF, we transected the axons of newborn rat motor neurons and demonstrated that iocal application of CNTF prevents the degeneration of the corresponding cell bodies.},
  language  = {en}
}
@article{ArakawaSendtnerThoenen1990,
  author    = {Arakawa, Yoshihiro and Sendtner, Michael and Thoenen, Hans},
  title     = {Survival effect of ciliary neurotrophic factor (CNTF) on chick embryonic motoneurons in culture: comparison with other neurotrophic factors and cytokines},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-31718},
  year      = {1990},
  abstract  = {No abstract available},
  language  = {en}
}
@article{LillienSendtnerRaff1990,
  author    = {Lillien, Laura E. and Sendtner, Michael and Raff, Martin C.},
  title     = {Extracellular Matrix-associated molecules collaborate with ciliary neurotrophic factor to induce type-2 astrocyte development},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42602},
  year      = {1990},
  abstract  = {0-2A progenitor cells give rise to both oligodendrocytes and type-2 astrocytes in vitro. Whereas oligodendrocyte differentiation occurs constitutively, type-2 astrocyte differentiation requires extracellular signals, one of which is thought to be ciliary neurotrophic factor (CNTF). CNTF, however, is insufficient by itself to induce the development of stable type-2 astrocytes. In this report we show the following: (a) that molecules associated with the extracellular matrix (ECM) cooperate with CNTF to induce stable type-2 astrocyte differentiation in serumfree cultures. The combination of CNTF and the ECM-associated molecules thus mimics the effect of FCS, which has been shown previously to induce stable type-2 astrocyte differentiation in vitro. (b) Both the ECM-associated molecules and CNTF act directly on 0-2A progenitor cells and can induce them to differentiate prematurely into type-2 astrocytes. (c) ECM-associated molecules also inhibit oligodendrocyte differentiation, even in the absence of CNTF, but this inhibition is not sufficient on its own to induce type-2 astrocyte differentiation. (d) Whereas the effect of ECM on oligodendrocyte differentiation is mimicked by basic fibroblast growth factor (bFGF), the effect of ECM on type-2 astrocyte differentiation is not. (e) The ECM-associated molecules that are responsible for inhibitin~ oligodendrocyte differentiation and for cooperating with CNTF to induce type-2 astrocyte differentiation are made by non-glial cells in vitro. (f) Molecules that have these activities and bind to ECM are present in the optic nerve at the time type-2 astrocytes are thought to be developing.},
  language  = {en}
}
@article{ErnsbergerSendtnerRohrer1989,
  author    = {Ernsberger, Uwe and Sendtner, Michael and Rohrer, Hermann},
  title     = {Proliferation and differentiation of embryonic chick sympathetic neurons: Effects of ciliary neurotropic factor.},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-31721},
  year      = {1989},
  abstract  = {At early developmental stages (embryonic day 7, E7), chick paravertebral sympathetic ganglia contain a cell population that divides in culture while expressing various neuronal properties. In an attempt to identify factors that control neuronal proliferation, we found that ciliary neurotrophic factor (CNTF) specifically inhibits the proliferation of those cells expressing neuronal markers. In addition, CNTF affects the differentiation of sympathetic ganglion cells by inducing the expression of vasoactive intestinal peptide immunoreactivity (VIP-IR). After 1 day in culture, tyrosine hydroxylase immunoreactivity (TH-I R) was expressed by about 86\% of the cells whereas VIP-IR was virtually absent. In the presence of CNTF, 50\%-60\% of the cells expressed VIP-IR after 4 days in culture; however, none of the cells expressed VIP-IR in the absence of CNTF. These results, and the demonstration of cells that express both VIP and TH-IR, indicate that VIP is induced in cells that initially express tyrosine hydroxylase. The findings suggest a potential role for CNTF as a factor affecting the proliferation and differentiation of developing sympathetic neurons.},
  language  = {en}
}
@article{BorasioJohnWittinghoferetal.1989,
  author    = {Borasio, Gian Domenico and John, Jacob and Wittinghofer, Alfred and Barde, Yves-Alain and Sendtner, Michael and Heumann, Rolf},
  title     = {ras p21 protein promotes survival and fiber outgrowth of cultured embryonic neurons},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-32621},
  year      = {1989},
  abstract  = {Although evidence obtained with the PC12 cell line has suggested a role for the ras oncogene proteins in the signal transduction of nerve growth factor-mediated fiber outgrowth, little is known about the signal transduction mechanisms involved in the neuronal response to neurotrophic factors in nontransformed cells. We report here that the oncogene protein T24-ras, when introduced into the cytoplasm of freshly dissociated chick embryonic neurons, promotes the in vitro survival and neurite outgrowth of nerve growth factor-responsive dorsal rootganglion neurons, brain-derived neurotrophic factor-responsive nodose ganglion neurons, and ciliary neuronotrophic factor-responsive ciliary ganglion neurons. The proto-oncogene product c-Ha-ras also promotes neuronal survival, albeit less strongly. No effect could be observed with truncated counterparts of T24-ras and c-Ha-ras lacking the 23 C-terminal amino acids including the membrane-an-choring, palmityl-accepting cysteine. These results sug-gest a generalized involvement of ras or ras-like proteins in the intracellular signal transduction pathway for neurotrophic factors.},
  language  = {en}
}
@article{StoeckliLottspeichSendtneretal.1989,
  author    = {St{\"o}ckli, K. A. and Lottspeich, F. and Sendtner, Michael and Masiakowski, P. and Carroll, Patrick and G{\"o}tz, Rudolf and Lindholm, D. and Thoenen, Hans},
  title     = {Molecular cloning, expression and regional distribution of rat ciliary neurotrophic factor},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-34229},
  year      = {1989},
  abstract  = {CILIARY neurotrophic factor (CNTF) was originally characterized as a survival factor for chick ciliary neurons in vitro. More recently, it was shown to promote the survival of a variety of otherneuronal cell types and to affect the differentiation of E7 chick sympathetic neurons by inhibiting their proliferation and by inducing the expression of yasoactiYe intestinal peptide immunoreactiyity (VIP-IR). In cultures of dissociated sympathetic neurons from newborn rats, CNTF induces cholinergic differentiation as shown by increased levels of choline acetyltransferase (ChAT.},
  language  = {en}
}
@article{SaadatSendtnerRohrer1989,
  author    = {Saadat, S. and Sendtner, Michael and Rohrer, H.},
  title     = {Ciliary neurotrophic factor induces cholinergic differentiation of rat sympathetic neurons in culture},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-32677},
  year      = {1989},
  abstract  = {Ciliary neurotrophic factor (CNTF) influences the levels of choline acetyltransferase (ChAT) and tyrosine hydroxylase (TH) in cultures of dissociated sYmpathetic neurons from newborn rats. In the presence of CNTF both the total and specific activity of ChAT was increased 7 d after culture by 15- and 18-fold, respectively, as compared to cultures kept in the absence of CNTF. Between 3 and 21 d in culture in the presence of CNTF . the total ChAT activity increased by a factor of >100. Immunotitration demonstrated that the elevated ChAT levels were due to an increased number of enzyme molecules. In contrast to the increase in ChAT levels, the total and specific activity levels' of TH were decreased by 42 and 36 \%, respectively, after 7 d in culture. Half-maximal effects for both ChAT increase and TH decrease were obtained at CNTF concentrations of rvO.6 ng and maximal levels were reached at I ng of CNTF per milliliter of medium. The effect of CNTF on TH and ChAT levels were seen in serum-containing medium as well as in serum-free medium. CNTF was shown to have only a small effect on the long-term s.urviVal of rat sympathetic neurons. We therefore concluded that the effects of CNTF on ChAT and TH are not due to selective survival of cells that acquire cholinergic traits in vitro, but are rather due to the induction of cholinergic differentiation of noradrenergic sympathetic neurons.},
  language  = {en}
}
@article{LillienSendtnerRohreretal.1988,
  author    = {Lillien, Laura E. and Sendtner, Michael and Rohrer, Hermann and Hughes, Simon M. and Raff, Martin C.},
  title     = {Type-2 Astrocyte Development in Rat Brain Cultures is initiated by a CNTF-like protein produced by type-1 astrocytes},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-31708},
  year      = {1988},
  abstract  = {No abstract available},
  language  = {en}
}
@article{HughesLillienRaffetal.1988,
  author    = {Hughes, Simon M. and Lillien, Laura E. and Raff, Martin C. and Rohrer, Hermann and Sendtner, Michael},
  title     = {Ciliary neurotrophic factor induces type-2 astrocyte differentiation in culture},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42660},
  year      = {1988},
  abstract  = {We have been studying a population of bipotential glial progenitor cells in the perinatal rat optic nerve and brain in an attempt to understand how cells choose between alternative fates in the developing mammalian central nervous system (CNS). This cell population gives rise initially to oligodendrocytes and then to type-2 astrocytes1 both of which apparently collaborate in sheathing axons in the CNS2,3. In vitro studies suggest that oligodendrocyte differentiation is the constitutive pathway of development for the oligodendrocyte-type-2-astrocyte (O-2A) progenitor cell4,5, whereas type-2 astrocyte differentiation depends on a specific inducing protein6. This protein is present in the developing optic nerve when type-2 astrocytes are differentiating and can induce 0-2A progenitor cells in vitro to express glial fibrillary acidic protein (GFAP)6, a marker of astrocyte differentiation7. Here we show that the type-2-astrocyte-inducing protein is similar or identical to ciliary neutrotrophic factor (CNTF)8,9, which promotes the survival of some types of peripheral neurons in vitro8, including ciliary ganglion neurons8,10. This suggests that CNTF, in addition to its effect on neurons, may be responsible for triggering type-2 astrocyte differentiation in the developing CNS.},
  language  = {en}
}
@article{SendtnerGnahnWakadeetal.1988,
  author    = {Sendtner, Michael and Gnahn, H. and Wakade, A. and Thoenen, Hans},
  title     = {Is activation of the Na\(^+\)K\(^+\) pump necessary for NGF-mediated neuronal survival?},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42610},
  year      = {1988},
  abstract  = {The ability of nerve growth factor to cause rapid activation of the Na+K+ pump of its responsive cells was examined by measuring the uptake of 86Rb+. A significant increase in 86Rb+ uptake in Ea chick dorsal root ganglion sensory neurons after NGF treatment was seen only if the cells had been damaged during the preparation procedure. Such damaged cells could not survive in culture in the presence of NGF, and undamaged cells that did survive in response to NGF exhibited no increased 86Rb+ uptake rate. Furthermore, cultured calf adrenal medullary cells did not show an increase in 86Rb+ uptake after treatment with NGF, although these cells respond to NGF with an increased synthesis of catecholaminergic enzymes. These results are incompatible with the hypothesis that the mechanism of action of NGF that promotes neuronal survival and enzyme induction results from an initial stimulation of the Na+K+ pump.},
  language  = {en}
}