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. 2001 Mar 15;21(6):1819–1829. doi: 10.1523/JNEUROSCI.21-06-01819.2001

Table 1.

Fits of dose–response data with empirical Hill equations

Chronic exposure to High-affinity state Low-affinity state Imax pA
(a1) EC50H (μm) nH1 (1 − a1) EC50L (μm) nH2
Control (59) 25  ± 1 1.5  ± 0.1 0.93  ± 0.01 75 61 ± 0.8 1.5 ± 0.04 2202  ± 273
8–10 hr 100 nm (−)-nicotine (8) 44  ± 5 1.4  ± 0.1 0.94  ± 0.03 56 61 1.5 3305  ± 448
19–23 hr 1 μm (−)-nicotine (5) 45  ± 5 2.1  ± 0.4 0.90  ± 0.03 55 61 1.5 4798  ± 606
19–23 hr 10 μm (−)-nicotine (7) 37  ± 6 1.4  ± 0.1 0.84  ± 0.03 63 61 1.5 3477  ± 341
8–10 hr 10 nm DHβE (7) 50  ± 6 1.1  ± 0.2 0.84  ± 0.03 50 61 1.5 4868  ± 878
8–24 hr 10 μm DHβE (16) 70  ± 5 0.67  ± 0.2 0.91  ± 0.06 30 61 1.5 6026  ± 539
8–10 hr 10 μm MLA (12) 57  ± 3 1.6  ± 0.2 0.97  ± 0.02 43 61 1.5 5326  ± 735
10–24 hr 20 μm cyclo control (10) 36  ± 3 1.5  ± 0.2 0.92  ± 0.04 64 61 1.5 3563  ± 645
10–24 hr 20 μm cyclo + DHβE 10 μm (11) 54  ± 3 0.9  ± 0.1 1  ± 0.05 46 61 1.5 6012  ± 515

Control cells, recorded alternately with cells chronically exposed to drugs, were pooled together because they presented few variations between experiments. Data points of the dose–response values measured for cells exposed to drugs were fitted as follows: the low-apparent affinity was fixed at 61 μm with a Hill coefficient of 1.5 (corresponding to the mean values of control cells), and the other parameters were adjusted to fit of the data.