@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{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}
}
@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{MasuWolfHoltmannetal.1993,
  author    = {Masu, Yasuo and Wolf, Eckhard and Holtmann, Bettina and Sendtner, Michael and Brem, Gottfried and Thoenen, Hans},
  title     = {Disruption of the CNTF gene results in motor neuron degeneration},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-33038},
  year      = {1993},
  abstract  = {CNTF is a cytosolic molecule expressed postnatally in myelinating Schwann cells and in a subpopulation of astrocytes. Although CNTF administration prevents lesion-mediated and genetically determined motor neuron degeneration, its physiological function remained elusive. Here it is reported that abolition of CNTF gene expression by homologous recombination results in a progressive atrophy and loss of motor neurons in adult mice, which is functionally reflected by a small but significant reduction in muscle strength.},
  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{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{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{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{CarrollSendtnerMeyeretal.1993,
  author    = {Carroll, Patrick and Sendtner, Michael and Meyer, Michael and Thoenen, Hans},
  title     = {Rat ciliary neurothrophic factor (CNTF): gene structure and regulation of mRNA levels in glial cell cultures.},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-31763},
  year      = {1993},
  abstract  = {The structure of the rat ciliary neurotrophic factor (CNTF) gene and the regulation ofCNTF mRNA levels in cultured glial cells were investigated. The rat mRNA is encoded by a simple two-exon transcription unit. Sequence analysis of the region upstream of the transcription start-site did not reveal a typical TATA-box consensus sequence. Low levels of CNTF mRNA were detected in cultured Schwann cells, and CNTF mRNA was not increased by a variety of treatments. Three-week-old astrocyteenriched cell cultures from new-born rat brain contained easily detectable CNTF mRNA. In astrocyte-enriched cultures, upregulation of CNTF mRNA levels was observed after treatment with IFN-gamma. CNTF mRNA levels were down-regulated in these cells by treatments that elevate intracellular cyclic AMP and by members of the fibroblast growth factor (FGF) family. The implications of these results for potential in vivo functions of CNTF are discussed.},
  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}
}