Nitric oxide is involved in taurine release in the mouse brain stem under normal and ischemic conditions |
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Authors: | P Saransaari S S Oja |
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Institution: | (1) Tampere Brain Research Center, Medical School, University of Tampere, Tampere, Finland;(2) The Centre for Laboratory Medicine and Department of Clinical Physiology and Nuclear Medicine, Tampere University Hospital, Tampere, Finland |
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Abstract: | Summary. Nitric oxide (NO) has been shown to regulate neurotransmitter release in the brain; both inhibitory and excitatory effects
have been seen. Taurine is essential for the development and survival of neural cells and protects them under cell-damaging
conditions. In the brain stem, it regulates many vital functions such as cardiovascular control and arterial blood pressure.
Now we studied the effects of the NO-generating compounds hydroxylamine (HA), S-nitroso-N-acetylpenicillamine (SNAP) and sodium
nitroprusside (SNP) on the release of preloaded 3H]taurine under normal and ischemic conditions in slices prepared from the mouse brain stem from developing (7-day-old) to
young adult (3-month-old) mice. In general, the effects of NO on the release were somewhat complex and difficult to explain,
as expected from the multifunctional role of NO in the central nervous system. The basal initial release under normal conditions
was enhanced by the NO donors 5 mM HA and 1.0 mM SNAP at both ages, but SNP was inhibitory in developing mice. The release
was markedly enhanced by K+ stimulation. The effects of HA, SNAP and SNP on the basal release were not antagonized by the NO synthase inhibitor NG-nitro-L-arginine (L-NNA, 1.0 mM), demonstrating that mechanisms other than NO synthesis are involved. Taurine release in
developing mice in the presence of SNP was reduced by the inhibitor of soluble guanylate cyclase, 1H-(1,2,3)oxadiazolo(4,3-a)quinoxalin-1-one
(ODQ), indicating the possible involvement of cGMP. In normoxia, N-methyl-D-aspartate (NMDA, 1.0 mM) enhanced the SNAP- and
HA-evoked taurine release in developing mice and the HA-evoked release in adults. In ischemia, both K+ stimulation and NMDA potentiated the NO-induced release, particularly in the immature mice, probably without the involvement
of the NO synthase or cGMP. The substantial release of taurine in the developing brain stem evoked by NO donors together with
NMDA might represent signs of important mechanisms against excitotoxicity which protect the brain stem under cell-damaging
conditions.
Authors’ address: Prof. Pirjo Saransaari, Brain Research Center, Medical School University of Tampere, Tampere, FIN-3 3014,
Finland |
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Keywords: | : Taurine release – Nitric oxide – Ischemia – Brain stem – Tissue slices – Adult and developing mouse |
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