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. 2003 Feb 15;23(4):1320–1328. doi: 10.1523/JNEUROSCI.23-04-01320.2003

Fig. 6.

Fig. 6.

ATP and BzATP induce an efflux of preloaded14C glutamate and 3H d-aspartate.A, 14C glutamate release induced by 6 min incubations in standard BSS (left) or Ca2+/Mg2+-free BSS (right). BzATP produced a greater response than ATP under both conditions (p < 0.05), and the effects of both agonists were amplified in the Ca2+/Mg2+-free BSS. Cultures used for 14C glutamate studies were pretreated with methionine sulfoximine and amino-oxyacetic acid to inhibit the metabolism of glutamate to other 14C-labeled compounds (see Materials and Methods). B, 3H d-aspartate release induced by 6 min incubations in standard BSS (left) or Ca2+/Mg2+-free BSS (right). The dose–response curves indicate that BzATP is a more potent agonist than ATP and that the effects of both agonists are amplified in Ca2+/Mg2+-free medium. C, The effect of ATP on 3Hd-aspartate release was amplified by the removal of both Mg2+ and Ca2+ but not by the removal of either cation alone. Values in each panel are means ± SE; n ≥ 6. +, With; −, without. **p < 0.01.