Members of several gene families influence survival of rat motoneurons in vitro and in vivo

Hughes, R. A.; Sendtner, Michael; Thoenen, H.

doi:10.1002/jnr.490360607

Cited by 276 publications

(191 citation statements)

References 72 publications

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“…Moreover, in the facial ne rve lesion paradigm, a lso NT -3 was found to have a rescue effect which, however, was smaller than that of BDNF (96). Very recently, a neuron rescue effect has also been observed in lesioned facial motoneurons after the administration of NT-4 (39 …”

Section: Neurotrophic Effects Of Members Of the Ngf Gene Familymentioning

confidence: 93%

“…In more recent experiments with rat motoneurons, a marked neurotrophic action of IG F -I has been observed, the maximal survival amounting to 50% at the halfmaximal concentration of 500 pg/ml (39). Moreover, IGF -I also exhibits a marked rescue effect in the newborn rat facial nerve lesion paradigm (39).…”

Section: Insulin-like Growth Factor Ugf-i)mentioning

confidence: 95%

“…Thus, LIF, interleukin-6, and oncostatin-M deserve a thorough evaluation as additional potential neurotrophic molecules for motoneurons. Indeed, in vitro and in vivo effects of LIF on motoneurons have been observed (34,39,58). However, the physiological relevance of these observations remains to be established, particularly in view of the fact that a first evaluation of LIF -/-mice did not show any changes in spinal motoneurons either at the morphological or functional levels (84).…”

Section: Thoenen Hughes and Sendtnermentioning

confidence: 99%

“…However, another member of the FGF gene family, FGF -5, seems to fulfill the prerequisites for a target-derived trophic factor for motoneurons. FGF -5 shows a potent survival effect on both chick and rat motoneurons (38,39). It is expressed in rat skeletal muscle from E15 to adulthood.…”

Section: Neurotrophic Effects Of the Members Of The Fibroblast Growthmentioning

confidence: 99%

“…Progress was predominantly determined by an improvement of the motoneuron cell culture procedures (3,10,12,33,34,39) and the identification of neurotrophic molecules in adult and/or embryonic skeletal muscles with already known neurotrophic actions on other populations of neurons in vitro and in vivo (3,13,34,36,38,39,45,54,58,80). The importance of appropriate culture systems for motoneurons is demonstrated by the fact that, for a long time, no single, defined molecule could be demonstrated to have a convincing trophic action on motoneurons.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Trophic Support of Motoneurons: Physiological, Pathophysiological, and Therapeutic Implications

Thoenen¹,

Hughes²,

Sendtner³

1993

Experimental Neurology

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Section: Neurotrophic Effects Of Members Of the Ngf Gene Familymentioning

confidence: 93%

Section: Insulin-like Growth Factor Ugf-i)mentioning

confidence: 95%

Section: Thoenen Hughes and Sendtnermentioning

confidence: 99%

Section: Neurotrophic Effects Of the Members Of The Fibroblast Growthmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Trophic Support of Motoneurons: Physiological, Pathophysiological, and Therapeutic Implications

Thoenen¹,

Hughes²,

Sendtner³

1993

Experimental Neurology

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An Electrophysiologic Model for Functional Assessment of Effects of Neurotrophic Factors on Facial Nerve Reinnervation

Byrne

Stuart

Fakhry³

et al. 2005

Archives of Facial Plastic Surgery

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To establish a sound objective model for assessing the effects of neurotrophic factors on facial nerve function after injury and to compare the effects of brainderived neurotrophic factor (BDNF) with its neutralizing antibody on facial nerve function after injury.Design: Prospective electrophysiologic analysis of recovery of function 4 weeks after axotomy involving facial nerve transection and primary end-to-end reanastomosis in adult rats and blind comparison with randomized intramuscular injection of either BDNF, monoclonal antibody to BDNF in neutralizing concentration, or control solution.Results: There were no statistically significant differences between groups in latencies, duration, amplitude, area, or conduction velocity before axotomy, and recorded conduction velocities were consistent with previously reported values, which suggests that the recordings were reliable and reproducible. After transection, there was a mean increase in latency 1 and decreases in latency 2, integrated average area, muscle action potential duration, amplitude, and conduction velocity for all 3 groups. When the groups were compared after transection, the anti-BDNF group showed a significant decrease in conduction velocity and muscle action potential duration (Kruskal-Wallis P = .01 and P = .008, respectively) compared with the other groups. There were no statistically significant differences in latencies, amplitude, or area among the groups. Conclusions:We have established an electrophysiologic model for objective assessment of facial nerve function in the rat. Future studies should combine functional electrophysiologic assessment and histologic examination to provide a more robust model for studying the effects of neurotrophic factors on facial nerve reinnervation and synkinesis.

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Immunocytochemical localization of TrkB in the central nervous system of the adult rat

et al. 1997

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The TrkB family of transmembrane proteins serve as receptors for brain-derived neurotrophic factor (BDNF), neurotrophin (NT)-4/5, and possibly NT-3, three members of the neurotrophin family of neurotrophic factors. In order to understand the potential roles played by these receptors, we have examined the distribution of the TrkB receptor proteins in the adult rat brain by using immunohistochemistry. Several different antisera, directed against either synthetic peptides corresponding to different regions of TrkB or a recombinant fusion protein comprising part of the extracellular domain, were generated. Each of these antisera was directed to epitopes found on all known TrkB isoforms (both the tyrosine kinase-possessing isoform and the truncated kinase-lacking isoforms). In addition, a commercially available antibody to the intracellular domain of TrkB was also used. Widespread and distinct staining was observed on the surface of neuronal cell bodies, axons, and dendrites in many structures, including the cerebral cortex, hippocampus, dentate gyrus, striatum, septal nuclei, substantia nigra, cerebellar Purkinje cells, brainstem and spinal motor neurons, and brainstem sensory nuclei. Staining was also observed in the pia matter, on a subpopulation of ependymal cells lining the cerebral ventricle wall, and other nonneuronal cells. The expression pattern of TrkB receptor protein suggests that TrkB plays a broad role in the central nervous system. In addition, the detection of TrkB immunoreactivity on cell bodies and dendrites is consistent with recent models suggesting that neurotrophins may be derived from presynaptic and/or autocrine sources in addition to the classical postsynaptic target.

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Members of several gene families influence survival of rat motoneurons in vitro and in vivo

Cited by 276 publications

References 72 publications

Trophic Support of Motoneurons: Physiological, Pathophysiological, and Therapeutic Implications

Trophic Support of Motoneurons: Physiological, Pathophysiological, and Therapeutic Implications

An Electrophysiologic Model for Functional Assessment of Effects of Neurotrophic Factors on Facial Nerve Reinnervation

Immunocytochemical localization of TrkB in the central nervous system of the adult rat

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