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Bonanno G, Vallebuona F, Donadini F, Fontana G, Fedele E, Raiteri M: Heterocarrier-mediated reciprocal modulation of glutamate and glycine release in rat cerebral cortex and spinal cord synaptosomes. Eur J Pharmacol. 1994 Jan 24;252(1):61-7.
The effects of glutamic acid (Glu) and glycine (Gly) on each others release were studied using rat brain cortex and spinal cord synaptosomes. Previously taken up [3H] Gly and [3H] D-aspartic acid ([3H] D-Asp) was employed as markers for Gly and Glu/Asp release, respectively. Glu enhanced the release of [3H] Gly (EC50 = 8.4 microM) from cortical synaptosomes. The effect of Glu was not mimicked by the glutamate receptor agonists N-methyl-D-aspartic acid (NMDA), kainic or quisqualic acid. The Glu effect was abolished by the Glu/Asp uptake inhibitor D-threo-hydroxy-aspartic acid and it was Na+ sensitive. D-Asp also increased [3H] Gly release (EC50 = 9.9 microM) and the effect was blocked by the Glu/Asp uptake inhibitor. In contrast to its effect in the cortex, Glu failed to increase the release of [3H] Gly from spinal cord synaptosomes. Gly enhanced the outflow of [3H] D-Asp from rat cerebral cortex and spinal cord synaptosomes (EC50 = 75.0 and 99.5 microM, respectively). Gly was much more potent a releaser of [3H] D-Asp in the spinal cord than in the cortex. The Gly effects were insensitive to strychnine or to 7-Cl-kynurenic acid, antagonists at the two known Gly receptors, but they were strongly Na+ dependent. Our results are compatible with the idea that high-affinity uptake systems specific for Glu/Asp or Gly are colocalized on the same nerve terminal in rat spinal cord and cerebral cortex.(ABSTRACT TRUNCATED AT 250 WORDS) |
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