Fig. 7.

Pharmacology of ATP-inducedd-aspartate release indicates action at P2X₇receptors. A, Standard BSS. B–D, Ca²⁺/Mg²⁺-free BSS.A, ATP-induced d-aspartate release is blocked by DIDS, by the P2 receptor antagonist PPADS, and by a 2 hr preincubation with the irreversible P2X₇-selective inhibitor Ox-ATP. B, ATP was ∼10-fold more potent in Ca²⁺/Mg²⁺-free medium than in standard medium (compare with A). The P2X₇receptor inhibitors also blocked ATP-induced d-aspartate release in Ca²⁺/Mg²⁺-free medium, whereas the P2X₁ antagonist suramin was ineffective.C, d-Aspartate release was induced by BzATP and ATP but not by agonists of other purinergic receptor subtypes.Adenosin, Adenosine; α,β-Me-ATP, α,β-methylene ATP. D, ATP-induced release was not attenuated by preloading with PDC to block glutamate uptake reversal, by preloading the astrocytes with the calcium chelator BAPTA, or by depleting cell calcium with preincubation in Ca²⁺-free medium containing EGTA and thapsigargin (Thapsig). Preincubations with PDC, BAPTA-AM, and EGTA/thapsigargin were performed at 37°C for 40 min and followed by exchange with Ca²⁺/Mg²⁺-free BSS before thed-aspartate release assay. Values in eachpanel are means ± SE; n ≥ 6. **p < 0.01.