@article{SendtnerStoeckliThoenenetal.1992,
  author    = {Sendtner, Michael and St{\"o}ckli, Kurt A. and Thoenen, Hans and Schmalbruch, H. and Carroll, P. and Kreutzberg, Georg W.},
  title     = {Ciliary neurotrophic factor prevents the degeneration of motor neurons in mouse mutant progressive motor neuronopathy},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42563},
  year      = {1992},
  abstract  = {CILIARY neurotrophic factor (CNTF) supports the survival of embryonic motor neurons in vitro and in vivo and prevents lesion-mediated degeneration of rat motor neuron~ during early post-natal stages. Here we report that CNTF greatly reduces all the functional and morphological changes in pmnlpmn mice5, an autosomal recessive mutant leading to progressive caudo-cranial motor neuron degeneration. The first manifestations of progressive motor neuronopathy in homozygous pmnl pmn mice become apparent in the hind limbs at the end of the third post-natal week and all the mice die up to 6 or 7 weeks after birth from respiratory paralysis. Treatment with CNTF prolongs- survival- and greatly Impoves motor function of these mice. Moreover, morphological manifestations, such as loss of motor axons in the phrenic nerve and degeneration of facial motor neurons, were greatly reduced by CNTF, although the treatment did not start until the first symptoms of the disease had already become apparent and substantial degenerative changes were already present. The protective and restorative effects of CNTF in this mouse mutant give new perspectives for the treatment of human degenerative motor neuron diseases with CNTF.},
  language  = {en}
}
@article{SendtnerThoenenHoltmannetal.1992,
  author    = {Sendtner, Michael and Thoenen, Hans and Holtmann, B. and Kohlbeck, R. and Barde, Y.-A.},
  title     = {Brain-derived neurotrophic factor prevents the death of motoneurons in newborn rats after nerve section},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42673},
  year      = {1992},
  abstract  = {Motoneurons innervating the skeletal musculature were among the first neurons shown to require the presence of their target cells to develop appropriatelyl,2. But the characterization of molecules allowing motoneuron survival has been difficult. Ciliary neurotrophic factor prevents the death of motoneurons3-6, but its gene is not expressed during development7. Although the presence of a neurotrophin receptor on developing motoneurons8-1O has suggested a role for neurotrophins, none could be shown to promote motoneuron survival in vitro3. We report here that brainderived neurotrophic factor can prevent the death of axotomized motoneurons in newborn rats, suggesting a role for this neurotrophin for motoneuron survival in vivo.},
  language  = {en}
}
@article{SendtnerStoeckliCarrolletal.1992,
  author    = {Sendtner, Michael and St{\"o}ckli, Kurt A. and Carroll, Patrick and Kreutzberg, Georg W. and Thoenen, Hans},
  title     = {More on motor neurons},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42598},
  year      = {1992},
  abstract  = {No abstract available},
  language  = {en}
}
@article{StoeckliLililienNaeherNoeetal.1991,
  author    = {St{\"o}ckli, K. A. and Lililien, L. E. and N{\"a}her- No{\´e}, M. and Breitfeld, G. and Hughes, Richard A. and Raff, M. C. and Thoenen, Hans and Sendtner, Michael},
  title     = {Regional distribution, developmental changes, and cellular localization of CNTF-mRNA and protein in the rat brain},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-31172},
  year      = {1991},
  abstract  = {Ciliary neurotrophic factor (CNTF) is a potent survival molecule for a variety of embryonic neurons in culture. The developmental expression of CNTF occurs clearly after the time period of the physiological cell death of CNTF-responsive neurons. This, together with the sites of expression, excludes CNTF as a target-derived neuronal survival factor, at least in rodents. However, CNTF also participates in the induction of type 2 astrocyte differentiation in vitro. Here we demonstrate that the time course of the expression of CNTF-mRNA and protein in the rat optic nerve (as evaluated by quantitative Northern blot analysis and biological activity, respectively) is compatible with such a glial differentiation function of CNTF in vivo. We also show that the type 2 astrocyte-inducing- activity previously demonstrated in optic nerve extract can be precipitated by an antiserum against CNTF. Immunohistochemical analysis of astrocytes in vitro and in vivo demonstrates that the expression of CNTF is confined to a subpopulation of type 1 astrocytes. The olfactory bulb of adult rats has comparably high levels of CNTF to the optic nerve, and here again, CNTF-immunoreactivity is localized in a subpopulation of astrocytes. However, the postnatal expression of CNTF in the olfactory bulb occurs later than in the optic nerve. In other brain regions both CNTF-mRNA and protein levels are much lower.},
  language  = {en}
}
@misc{SendtnerArakawaStoecklietal.1991,
  author    = {Sendtner, Michael and Arakawa, Yoshihiro and St{\"o}ckli, Kurt A. and Kreutzberg, Georg W. and Thoenen, Hans},
  title     = {Effect of ciliary neurotrophic factor (CNTF) on motoneuron survival},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-33048},
  year      = {1991},
  abstract  = {We have demonstrated that the extensive degeneration of motoneurons in the rat facial nucleus after transection of the facial nerve in newborn rats can be prevented by local ciliary neurotrophic factor (CNTF) administration. CNTF differs distinctly from known neurotrophic molecules such as NGF, BDNF and NT-3 in both its molecular characteristics (CNTF is a cytosolic rather than a secretory molecule) and its broad spectrum of biological activities. CNTF is expressed selectively by Schwann cells and astrocytes of the peripheral and central nervous system, respectively, but not by target tissues of the great variety of CNTF -responsive neurons. CNTF mRNA is not detectable by Northern blot or PCR analysis during embryonic development and immediately after birth. However, during the second post-natal week, a more than 30-fold increase in CNTF mRNA and pro tein occurs in the sciatic nerve. Since the period of low CNTF levels in peripheral nerves coincides with that of high vulnerability of motoneurons (i.e. axonallesion results in degeneration of motoneuron cell bodies), insufficient availability of CNTF may be the reason for the rate of lesioninduced cell death of early post-natal motoneurons. Highly enriched embryonic chick motoneurons in culture are supported at survival rates higher than 60\% by CNTF, even in single cell cultures, indicating that CNTF acts directly on motoneurons. In contrast to CNTF, the members of the neurotrophin gene family (NGF, BDNF and NT-3) do not support the survival of motoneurons in culture. However, aFGF and bFGF show distinct survival activities which are additive to those of CNTF, resulting in the survival of virtually all motoneurons cultured in the presence of CNTF and bFGF.},
  language  = {en}
}
@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{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{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}
}
@article{DohrmannEdgarSendtneretal.1986,
  author    = {Dohrmann, Ulrike and Edgar, David and Sendtner, Michael and Thoenen, Hans},
  title     = {Muscle-derived factors that support survival and promote fiber outgrowth from embryonic chick spinal motor neurons in culture},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-72862},
  year      = {1986},
  abstract  = {The purpose of the experiments reported is to provide an unambiguous demonstration that embryonie skeletal muscle contains factors that act directly on embryonie spinal motor neurons both to support their survival and to stimulate the outgrowth of neurites. Cells of lumbar and brachial ventral spinal cords from 6-day-old chick embryos were separated by centrifugation in a two-step metrizamide gradient, and a motor neuron enriched fraction was obtained. Motor neurons were identified by retrogradely labeling with rhodamine isothiocyanate, and were enriched fourfold in the motor neuron fraction relative to unfractionated cells. In culture, the isolated motor neurons died within 3-4 days unless they were supplemented with embryonie chick skeletal muscle extract. Two functionally distinct entities separable by ammonium sulfate precipitation were responsible for the effects of muscle extracts on motor neurons. The 0-25\% ammonium sulfate precipitate contained molecules that alone bad no effect on neuronal survival but when bound to polyornithine-coated culture substrata, stimulated neurite outgrowth and potentiated the survival activity present in muscle. Most of this activity was due to a laminin-like molecule being immunoprecipitated with antisera against laminin, and immunoblotting demonstrated the presence of both the A and B chains of laminin. A long-term survival activity resided in the 25-70\% ammonium sulfate fraction, and its apparent total and specific activities were strongly dependent on the culture substrate. In contrast to the motor neurons, the cells from the other metrizamide fraction (including neuronal cells) could be kept in culture for a prolonged time without addition of exogenous factor(s).},
  subject      = {Nervenzelle},
  language  = {en}
}