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GABA A receptor in growth cones: The outline of GABA A receptor‐dependent signaling in growth cones is applicable to a varitey of α‐subunit species
Author(s) -
Fukura Haruhiko,
Kitani Yasuharu,
Komiya Yoshiaki,
Igarashi Michihiro
Publication year - 1999
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/(sici)1097-4547(19991101)58:3<407::aid-jnr6>3.0.co;2-k
Subject(s) - gabaa receptor , growth cone , protein subunit , microbiology and biotechnology , signal transduction , biology , gabaa rho receptor , receptor , chemistry , biochemistry , axon , gene
The growth cone is responsible for axonal elongation and pathfinding by responding to various modulators for neurite growth, including neurotransmitters. We demonstrated an outline of the gamma aminobutyric acid (GABA) A ‐dependent signaling in growth cones. Here, we examined the effects of the modulators of GABA A receptor on the signaling in growth cones. Phenobarbital or propofol, acting on β‐subunit, enhanced the [Cl ‐ ]infi change and [Ca 2+ ] i elevation by the GABA stimulation to isolated growth cones. Besides, propofol enhanced GABA‐dependent phosphorylation of growth‐associated protein of 43 kDa (GAP‐43) by protein kinase C. In contrast, an α‐subunit acting agent diazepam did not modulate any of the above signals. Next, we examined the effect of the developmental change of α‐subunit on the outline of the GABA A ‐dependent signaling in growth cones. We also found that the amounts of several different α‐subunit isoforms developmentally increased or decreased in growth cone membrane (GCM), but that the affinity and density of the [ 3 H]diazepam binding sites were similar to those in adult synaptic membrane. Taken together, our results strongly suggest that each step of GABA A ‐dependent signaling in GCM is not modified by diazepam, indicating that the signaling pathway mediated by GABA A receptor in growth cones is applicable to any compositional change of α‐subunit isoforms. J. Neurosci. Res. 58:407–416, 1999. © 1999 Wiley‐Liss, Inc.