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Peripheral facial nerve axotomy in mice causes sprouting of motor axons into perineuronal central white matter: time course and molecular characterization.

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Peripheral facial nerve axotomy in mice causes sprouting of motor axons into perineuronal central white matter: time course and molecular characterization.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Makwana, Milan Werner, Alexander Acosta-Saltos, Alejandro Gonitel, Roman Pararajasingam, Abirami Pararajasingham, Abirami Ruff, Crystal Rumajogee, Prakasham Cuthill, Dan Galiano, Mathias Bohatschek, Marion Wallace, Adam S. Anderson, Patrick N. Mayer, Ulrike Behrens, Axel Raivich, Gennadij
Description	Country affiliation: United kingdom Author Affiliation: Makwana M ( Department of Obstetrics and Gynaecology, EGA Institute for Women's Health, University College London, United Kingdom.)
Abstract	Generation of new axonal sprouts plays an important role in neural repair. In the current study, we examined the appearance, composition and effects of gene deletions on intrabrainstem sprouts following peripheral facial nerve axotomy. Axotomy was followed by the appearance of galanin(+) and calcitonin gene-related peptide (CGRP)(+) sprouts peaking at day 14, matching both large, neuropeptide(+) subpopulations of axotomized facial motoneurons, but with CGRP(+) sprouts considerably rarer. Strong immunoreactivity for vesicular acetylcholine transporter (VAChT) and retrogradely transported MiniRuby following its application on freshly cut proximal facial nerve stump confirmed their axotomized motoneuron origin; the sprouts expressed CD44 and alpha7beta1 integrin adhesion molecules and grew apparently unhindered along neighboring central white matter tracts. Quantification of the galanin(+) sprouts revealed a stronger response following cut compared with crush (day 7-14) as well as enhanced sprouting after recut (day 8 + 6 vs. 14; 14 + 8 vs. 22), arguing against delayed appearance of sprouting being the result of the initial phase of reinnervation. Sprouting was strongly diminished in brain Jun-deficient mice but enhanced in alpha7 null animals that showed apparently compensatory up-regulation in beta1, suggesting important regulatory roles for transcription factors and the sprout-associated adhesion molecules. Analysis of inflammatory stimuli revealed a 50% reduction 12-48 hours following systemic endotoxin associated with neural inflammation and a tendency toward more sprouts in TNFR1/2 null mutants (P = 10%) with a reduced inflammatory response, indicating detrimental effects of excessive inflammation. Moreover, the study points to the usefulness of the facial axotomy model in exploring physiological and molecular stimuli regulating central sprouting.
File Format	HTM / HTML
ISSN	00219967
e-ISSN	10969861
DOI	10.1002/cne.22240
Journal	Journal of Comparative Neurology
Issue Number	5
Volume Number	518
Language	English
Publisher	Wiley
Publisher Date	2010-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Neurology Facial Nerve Injuries Physiopathology Facial Nerve Physiology Growth Cones Ultrastructure Motor Neurons Nerve Regeneration Neuronal Plasticity Animals Axotomy Calcitonin Gene-related Peptide Metabolism Cell Adhesion Molecules Galanin Gene Deletion Immunohistochemistry Integrins Genetics Mice Mice, Knockout Mice, Transgenic Oncogene Protein P65(gag-jun) Receptors, Tumor Necrosis Factor, Type I Receptors, Tumor Necrosis Factor, Type Ii Time Factors Vesicular Acetylcholine Transport Proteins Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Neuroscience

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Peripheral Facial Nerve Axotomy in Mice Causes Sprouting of Motor Axons Into Perineuronal Central White Matter: Time Course and Molecular Characterization

Peripheral Facial Nerve Axotomy in Mice Causes Sprouting of Motor AxonsInto Perineuronal Central White Matter: Time Course and MolecularCharacterization

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Peripheral facial nerve axotomy in mice causes sprouting of motor axons into perineuronal central white matter: time course and molecular characterization.

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