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GABA and its B-receptor are present at the node of Ranvier in a small population of sensory fibers, implicating a role in myelination
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Organismal Biology.
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2015 (English)In: Journal of Neuroscience Research, ISSN 0360-4012, E-ISSN 1097-4547, Vol. 93, no 2, 285-295 p.Article in journal (Refereed) Published
Abstract [en]

The γ-aminobutyric acid (GABA) type B receptor has been implicated in glial cell development in the peripheral nervous system (PNS), although the exact function of GABA signaling is not known. To investigate GABA and its B receptor in PNS development and degeneration, we studied the expression of the GABAB receptor, GABA, and glutamic acid decarboxylase GAD65/67 in both development and injury in fetal dissociated dorsal root ganglia (DRG) cell cultures and in the rat sciatic nerve. We found that GABA, GAD65/67, and the GABAB receptor were expressed in premyelinating and nonmyelinating Schwann cells throughout development and after injury. A small population of myelinated sensory fibers displayed all of these molecules at the node of Ranvier, indicating a role in axon-glia communication. Functional studies using GABAB receptor agonists and antagonists were performed in fetal DRG primary cultures to study the function of this receptor during development. The results show that GABA, via its B receptor, is involved in the myelination process but not in Schwann cell proliferation. The data from adult nerves suggest additional roles in axon-glia communication after injury.

Place, publisher, year, edition, pages
2015. Vol. 93, no 2, 285-295 p.
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Neurosciences
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URN: urn:nbn:se:uu:diva-238740DOI: 10.1002/jnr.23489ISI: 000346475600008PubMedID: 25327365OAI: oai:DiVA.org:uu-238740DiVA: diva2:772066
Available from: 2014-12-16 Created: 2014-12-16 Last updated: 2017-12-05Bibliographically approved

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Wicher, GrzegorzFredriksson, Robert

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Department of NeuroscienceDepartment of Immunology, Genetics and PathologyDepartment of Organismal BiologyFunctional Pharmacology
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