Fig. 4.
Fig. 4. Ca++ mobilization of transfected P2X1wt and P2X1del receptors. / (A) Dose-response Ca++ influx (rate of fluorescence increase at 510 nm) for the P2X1wt receptor (summarized for P2X1wt clones designated W1, W2, W3, and W4) exposed to ATP (●, 2-6 individual experiments per concentration) or ADP (■, 2-7 individual experiments per concentration). (B) Dose-response Ca++ influx for the P2X1del receptor (summarized for P2X1del clones designated DL1, DL3, DL4, and DL5) exposed to ATP (●, 2-14 individual experiments per concentration) or ADP (■, 2-16 individual experiments per concentration). Values shown in panels A and B are mean ± SD (C) Ca++ influx profiles for the P2X1del receptor exposed to differing concentrations of ATP. A delayed activation by ATP is observable only at concentrations of 3 μM (trace 3) or greater. (D) Ca++ influx profiles for the P2X1delreceptor exposed to differing concentrations of ADP. Ca++influx is evident at concentrations of 0.3 μM (trace 1) or greater. Transfected cells expressing P2X1del receptors were exposed to increasing concentrations (0.3, 1, 3, or 10 μM, traces 1-4, respectively) of ATP (C) or ADP (D). Note that although the P2X1wt receptor is activated at similar concentrations by both ATP and ADP, the P2X1del receptor is activated to a greater extent by ADP at all concentrations. No activation was observed by either ATP or ADP in the absence of exogenous Ca++ or using nontransfected 1321 cells, confirming both the absence of endogenously activated nucleotide receptors and the requirement for influx of Ca++ as expected for an ion channel functioning as a receptor. (E) Ca++ influx profile for the P2X1wt receptor with the sequential addition of agonists. ATP (30 μM), ADP (30 μM), and carbachol (C, 50 μM) were added as indicated. (F) Ca++ influx profile for the P2X1del receptor with the sequential addition of agonists. ADP (30 μM), ATP (30 μM), and carbachol (C, 50 μM) were added as indicated. Note the different x-axis values between panels E or F (200 seconds) and C or D (40 seconds).

Ca++ mobilization of transfected P2X1wt and P2X1del receptors.

(A) Dose-response Ca++ influx (rate of fluorescence increase at 510 nm) for the P2X1wt receptor (summarized for P2X1wt clones designated W1, W2, W3, and W4) exposed to ATP (●, 2-6 individual experiments per concentration) or ADP (■, 2-7 individual experiments per concentration). (B) Dose-response Ca++ influx for the P2X1del receptor (summarized for P2X1del clones designated DL1, DL3, DL4, and DL5) exposed to ATP (●, 2-14 individual experiments per concentration) or ADP (■, 2-16 individual experiments per concentration). Values shown in panels A and B are mean ± SD (C) Ca++ influx profiles for the P2X1del receptor exposed to differing concentrations of ATP. A delayed activation by ATP is observable only at concentrations of 3 μM (trace 3) or greater. (D) Ca++ influx profiles for the P2X1delreceptor exposed to differing concentrations of ADP. Ca++influx is evident at concentrations of 0.3 μM (trace 1) or greater. Transfected cells expressing P2X1del receptors were exposed to increasing concentrations (0.3, 1, 3, or 10 μM, traces 1-4, respectively) of ATP (C) or ADP (D). Note that although the P2X1wt receptor is activated at similar concentrations by both ATP and ADP, the P2X1del receptor is activated to a greater extent by ADP at all concentrations. No activation was observed by either ATP or ADP in the absence of exogenous Ca++ or using nontransfected 1321 cells, confirming both the absence of endogenously activated nucleotide receptors and the requirement for influx of Ca++ as expected for an ion channel functioning as a receptor. (E) Ca++ influx profile for the P2X1wt receptor with the sequential addition of agonists. ATP (30 μM), ADP (30 μM), and carbachol (C, 50 μM) were added as indicated. (F) Ca++ influx profile for the P2X1del receptor with the sequential addition of agonists. ADP (30 μM), ATP (30 μM), and carbachol (C, 50 μM) were added as indicated. Note the different x-axis values between panels E or F (200 seconds) and C or D (40 seconds).

Close Modal
This Feature Is Available To Subscribers Only

or Create an Account

Close Modal
Close Modal