@article{SendtnerCarrollHoltmannetal.1994,
  author    = {Sendtner, Michael and Carroll, P. and Holtmann, B and Hughes, R. A. and Thoenen, H.},
  title     = {Ciliary Neurotrophic Factor},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-42545},
  year      = {1994},
  abstract  = {No abstract available},
  language  = {en}
}
@article{SendtnerDittrichHughesetal.1994,
  author    = {Sendtner, Michael and Dittrich, F. and Hughes, R. A. and Thoenen, H.},
  title     = {Actions of CNTF and neurotrophins on degenerating motoneurons : preclinical studies and clinical implications},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-62939},
  year      = {1994},
  abstract  = {Spinal motoneurons innervating skeletal muscle were amongst the first neurons shown to require the presence of their target cells to develop appropriately. Isolated embryonie chick and rat motoneurons have been used to identify neurotrophic factors and cytokines capable of supporting the survival of developing motoneurons. Such factors include ciliary neurotrophic factor (CNTF), which is present physiologically in high amounts in myelinating Schwann cells of peripheral nerves, and brain-derived neurotrophic factor (BDNF) which is synthesized in skeletal muscle and, after peripheral nerve lesion. in Schwann cells. These factors have been further analyzed for their physiological significance in maintaining motoneuron function in vivo, and for their potential therapeutic usefulness in degenerative motoneuron disease. Both CNTF and BDNF are capable of rescuing injured facial motoneurons in newbom rats. Furthermore, CNTF prolongs survival and improves motor function of pmn mice, an animal model for degenerative motoneuron disease, by preventing degeneration of motoneuron axons and somata. Thus treatment of human motoneuron disease with neurotrophic factors should be possible, provided that rational means for application of these factors can be established considering also the appearance of potential side effects.},
  subject      = {Neurobiologie},
  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{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{SendtnerStoeckliThoenen1992,
  author    = {Sendtner, Michael and St{\"o}ckli, K. A. and Thoenen, Hans},
  title     = {Synthesis and localization of ciliary neurotrophic factor in the sciatic nerve of the adult rat after lesion and during regeneration},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-31738},
  year      = {1992},
  abstract  = {Ciliary neurotrophic factor (CNTF) is expressed in high quantities in Schwann cells of peripheral nerves during postnatal development of the rat. The absence of a hydrophobic leader sequence and the immunohistochemical localization of CNTF within the cytoplasm of these cells indicate that the factor might not be available to responsive neurons under physiological conditions. However, CNTF supports the survival of a variety of embryonic neurons, including spinal motoneurons in culture. Moreover we have recently demonstrated that the exogenous application of CNTF protein to the lesioned facial nerve of the newborn rat rescued these motoneurons from cell death. These results indicate that CNTF might indeed play a major role in assisting the survival of lesioned neurons in the adult peripheral nervous system. Here we demonstrate that the CNTF mRNA and protein levels and the manner in which they are regulated are compatible with such a function in lesioned peripheral neurons. In particular, immunohistochemical analysis showed significant quantities of CNTF at extracellular sites after sciatic nerve lesion. Western blots and determination of CNTF biological activity of the same nerve segments indicate that extracellular CNTF seems to be biologically active. After nerve lesion CNTF mRNA levels were reduced to <5 \% in distal regions of the sciatic nerve whereas CNTF bioactivity decreased to only one third of the original before-lesion levels. A gradual reincrease in Schwann cells occurred concomitant with regeneration.},
  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{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{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}
}