@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}
}
@article{GoetzKoesterWinkleretal.1994,
  author    = {G{\"o}tz, Rudolf and K{\"o}ster, Reinhard and Winkler, Christoph and Raulf, Friedrich and Lottspeich, Friedrich and Schartl, Manfred and Thoenen, Hans},
  title     = {Neurotrophin-6 is a new member of the nerve growth factor family},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-61544},
  year      = {1994},
  abstract  = {DURING vertebrale development, many neurons depend for survival and differentiation on their target cells\(^{1-3}\). The best documented mediator of such a retrograde trophic action is the neurotrophin nerve growth factor (NGF)\(^1\). NGF and the other known members of tbe neurotrophin family, brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT -3) and neurotrophin-4/5 (NT -4/5) are conserved as distinct genes over large evolutionary distances\(^{4 -6}\). Here we report the cloning of neurotrophin-6 (NT -6), a new member of this family from the teleost fish Xiphophorus. NT -6 distinguishes itself from the other known neurotrophins in that it is not found as a soluble protein in the medium of producing cells. The addition of heparin (but not chondroitin) effects the release of NT -6 from cell surface and extracellular matrix molecules. Recombinant purified NT -6 has a spectrum of actions similar to NGF on chick sympathetic and sensory neurons, albeit with a lower potency. NT -6 is expressed in tbe embryonie valvulla cerebelli; expression persists in some adult tissues. The interaction of NT-6 with heparin-binding molecuJes may modulate its action in the nervous system .},
  subject      = {Physiologische Chemie},
  language  = {en}
}
@article{SendtnerThoenen1994,
  author    = {Sendtner, Michael and Thoenen, Hans},
  title     = {Oxidative stress and motorneuron disease},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42684},
  year      = {1994},
  abstract  = {Transgenic mice carrying mutated Cu/Zn superoxide dismutase genes provide insights into the pathogenesis of human motorneuron diseases and may be useful as models in the development and testing of therapies.},
  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{SendtnerThoenenHughes1993,
  author    = {Sendtner, Michael and Thoenen, Hans and Hughes, R. A.},
  title     = {Members of several gene families influence survival of rat motoneurons in vitro and in vivo},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42652},
  year      = {1993},
  abstract  = {The survival and functional maintenance of spinal motoneurons, both during the period of developmental cell death and in adulthood, have been shown to be dependent on trophic factors. In vitro experiments have previously been used to identify several survival factors for motoneurons, including CNTF, UF, and members of the neurotrophin, FGF, and IGF gene families. Some of these factors have also been shown to be active in vivo, either on chick motoneurons during embryonic development or on lesioned facial and spinal motoneurons of the newborn rat. Here we demonstrate that lesioned newborn rat facial motoneurons can be rescued by NT-4/5, IGF-I, and UF. Furthermore, in contrast to chick motoneurons, the survival of isolated embryonic rat motoneurons can be maintained by the neurotrophins BDNF, NT-3, and NT-4/5. IGF-I and FGF-5 were also active in this system, each supporting more than 50\% of the originally plated neurons. The responsiveness of motoneurons to multiple factors in vitro and in vivo suggests that motoneuron survival and function are regulated by the coordinated actions of members of different gene families.},
  language  = {en}
}
@article{DittrichThoenenSendtner1994,
  author    = {Dittrich, Falk and Thoenen, Hans and Sendtner, Michael},
  title     = {Ciliary neurotrophic factor: pharmacokinetics and acute-phase response in rat},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42639},
  year      = {1994},
  abstract  = {No abstract available},
  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{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{HughesSendtnerGoldfarbetal.1993,
  author    = {Hughes, Richard A. and Sendtner, Michael and Goldfarb, Mitchell and Lindholm, Dan and Thoenen, Hans},
  title     = {Evidence that fibroblast growth factor 5 is a major muscle-derived survival factor for cultured spinal motoneurons},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42588},
  year      = {1993},
  abstract  = {We examined the potential role of fibroblast growth factor 5 (FGF-5) as a target-derived trophic factor for spinal motoneurons. Northern analysis of total RNA from rat skeletal muscle revealed an FGF-5 mRNA transcript both during the period of embryonic motoneuron death and in the adult. Recombinant human FGF-5 supported the survival of highly enriched cultures of embryonic chick motoneurons. Significant proportions of the motoneuron survival activity of rat skeletal muscle extracts could be immunoprecipitated using an antiserum to FGF-5. The immunoprecipitable activity was present in soluble and matrix-bound forms in embryonic muscle, but bound exclusively to the extracellular matrix in adult muscle. These results, along with the secretory nature of FGF-5, suggest that FGF-5 may act as a target-derived trophic factor for motoneurons.},
  language  = {en}
}
@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}
}