NDLI: Characteristics of GABA Release Induced by Free Radicals in Mouse Hippocampal Slices

Content Provider	Springer Nature Link
Author	Saransaari, Pirjo Oja, Simo S.
Copyright Year	2007
Abstract	The release of the inhibitory neurotransmitter GABA is generally enhanced under potentially cell-damaging conditions. The properties and regulation of preloaded [$^{3}$H]GABA release from mouse hippocampal slices were now studied in free radical-containing medium in a superfusion system. Free radical production was induced by 0.01% of H$_{2}$O$_{2}$ in the medium. H$_{2}$O$_{2}$ markedly potentiated GABA release, which was further enhanced about 1.5-fold by K$^{+}$ stimulation (50 mM). In Ca$^{2+}$-free media this stimulation was not altered, indicating that the release was mostly Ca$^{2+}$-independent. Moreover, omission of Na$^{+}$ increased the release, suggesting that it is mediated by Na$^{+}$-dependent transporters operating outwards, a conception confirmed by the enhancement with GABA homoexchange. Inhibition of the release with the ion channel inhibitors diisothiocyanostilbene-2,2′-disulphonate and 4-acetamido-4′-isothiocyanostilbene-2,2′-disulphonate indicates that Cl$^{−}$ channels also participate in the process. This release was not modified by the adenosine receptor (A$_{1 }$and A$_{2a}$) agonists and ionotropic glutamate receptor agonists kainate, N-methy-d-aspartate and 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate, whereas the agonists of metabotropic glutamate receptors of group I [(S)-3,5-dihydroxyphenylglycine] and of group II [(2R,4R)-4-aminopyrrolidine-2,4-dicarboxylate] enhanced it by receptor-mediated mechanisms, the effects being abolished by their respective antagonists. The group III agonist l(+)-2-amino-4-phosphonobutyrate reduced the evoked GABA release, but this was not affected by the antagonist. Furthermore, the release was reduced by activation of protein kinase C by 4β-phorbol 12-myristate 13-acetate and by inhibition of tyrosine kinase by genistein and of phoshoplipase by quinacrine. On the other hand, increasing cGMP levels with the phosphodiesterase inhibitor zaprinast, selective for PDE5, 6 and 9, and NO production with the NO-generating compounds hydroxylamine, sodium nitroprusside and S-nitroso-N-penicillamine enhanced the release. The regulation of GABA release induced by free radical production proved thus to be rather complex. Under potentially cell-damaging conditions, the potentiation of GABA release may be a mechanism to counteract hyperactivity and reduce the effects of excitatory amino acid release. On the other hand, reduction of GABA release could be harmful and contribute to excitotoxic damage and neuronal degeneration.
Starting Page	384
Ending Page	393
Page Count	10
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	33
Issue Number	3
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2007-08-22
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Hippocampus Tissue slices GABA release Free radicals Cell damage Release mechanisms Neurology Biochemistry Neurosciences
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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