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GABA and its B‐receptor are present at the node of R anvier in a small population of sensory fibers, implicating a role in myelination
Author(s) -
Corell Mikael,
Wicher Grzegorz,
Radomska Katarzyna J.,
Dağlıkoca E. Duygu,
Godskesen Randi Elberg,
Fredriksson Robert,
Benedikz Eirikur,
Magnaghi Valerio,
Fex Svenningsen Åsa
Publication year - 2015
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.23489
Subject(s) - gabab receptor , schwann cell , receptor , sciatic nerve injury , axon , biology , population , neuroscience , microbiology and biotechnology , glutamate decarboxylase , peripheral nervous system , gabaa receptor , chemistry , central nervous system , biochemistry , medicine , regeneration (biology) , environmental health , enzyme
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 GABA B 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 GABA B 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 GABA B 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. © 2014 Wiley Periodicals, Inc.