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  Regulation, cellular localization, and function of the p75 neurotrophin receptor (p75NTR) during the regeneration of facial motoneurons

Gschwendtner, A., Liu, Z. Q., Hucho, T., Bohatschek, M., Kalla, R., Dechant, G., et al. (2003). Regulation, cellular localization, and function of the p75 neurotrophin receptor (p75NTR) during the regeneration of facial motoneurons. Molecular and Cellular Neuroscience, 24(2), 307-322. doi:10.1016/S1044-7431(03)00167-2.

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Gschwendtner, A.1, Author           
Liu, Z. Q.1, Author           
Hucho, T.2, Author
Bohatschek, M.1, Author           
Kalla, R.1, Author           
Dechant, Georg3, Author           
Raivich, G.1, Author           
Affiliations:
1Emeritus Group: Neuromorphology / Kreutzberg, MPI of Neurobiology, Max Planck Society, ou_1113551              
2Univ Coll London, Dept Anat, Dept Obstet & Gynecol, Perinatal Brain Repair Grp, London WC1E 6HX, England.; Max Planck Isnt Neurobiol, Dept Neuromorphol, D-82152 Martinsried, Germany.; Max Planck Isnt Neurobiol, Dept Neurobiochem, D-82152 Martinsried, Germany.; Innsbruck Univ, Dept Neurosci, A-6020 Innsbruck, Austria., ou_persistent22              
3Department: Neurobiochemie / Barde, MPI of Neurobiology, Max Planck Society, ou_3377529              

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 Abstract: The common neurotrophin receptor (p75NTR) is a member of the tumor necrosis factor receptor superfamily and binds the neurotrophins nerve growth factor, brain derived neurotrophic factor, neurotrophin-3, and neurotrophin-4. P75NTR is expressed on developing motoneurons and is reexpressed on adult motoneurons under pathological conditions such as nerve trauma or neurodegeneration. Here we examined the regulation and function of p75NTR during regeneration after peripheral transection of the facial nerve of adult mice. Axotomy led to a strong increase in p75NTR immunoreactivity on the injured and regenerating facial motoneurons and on denervated Schwann cells. Cellular colocalization also revealed p75NTR immunoreactivity on neighboring blood vessels and cells in the injured nerve, but not on activated GFAP+ astrocytes or alphaMbeta2+ microglia and macrophages. To determine the function of this receptor we examined the effects of p75NTR deficiency on neuroglial activation, on the speed of axonal regeneration, and on neuronal survival after facial axotomy in two different transgenic mouse lines carrying targeted insertions exon 4 (p75e4-/-) or exon 3 (p75e3-/-) of the p75NTR gene. In both animal models absence of p75NTR led to a twofold, early increase in the number of CD3+. T-cells and in the microglial immunoreactivity for the alpha5beta1, alpha6beta1, and alphaMbeta2 integrins at day 4 in the facial nucleus and in the crushed facial motor nerve. No changes were observed in the number of reactive GFAP+ astrocytes or on late microglial and lymphocyte responses. The rate of axonal elongation in the crushed facial nerve, as well as neuronal survival, was found to be unaffected. Overall, the current study shows that the p75NTR receptor plays an important regulatory role in early neuroglial and immune activation. (C) 2003 Elsevier Inc. All rights reserved.

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Language(s): eng - English
 Dates: 2003-10
 Publication Status: Published in print
 Pages: -
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 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 127708
ISI: 000186164400005
DOI: 10.1016/S1044-7431(03)00167-2
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Title: Molecular and Cellular Neuroscience
Source Genre: Journal
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Publ. Info: Orlando, Fla. : Academic Press
Pages: - Volume / Issue: 24 (2) Sequence Number: - Start / End Page: 307 - 322 Identifier: ISSN: 1044-7431
CoNE: https://pure.mpg.de/cone/journals/resource/954922650153