Table 3.

Inhibition by cocaine of m-tyramine-induced DA efflux as a function of DA concentrations

Initial [DA]o(μm)	[DA]o at steady state (nm)	[DA]i at steady state (μm)	IC50(μm)3-a	Ki(μm)3-a
	n = 12	n = 4	n = 3	n = 3
0.5	23  ± 4	44	11.6  ± 0.6	2.05  ± 0.07
1.0	27  ± 5	84	12.2  ± 0.6	2.23  ± 0.16
1.5	44  ± 3	124	12.9  ± 1.3	2.17  ± 0.04
2.0	88  ± 8	163	12.4  ± 0.8	2.15  ± 0.11
3.0	184  ± 15	242	11.0  ± 1.2	2.22  ± 0.12
4.0	359  ± 38	321	13.4  ± 1.5	2.47  ± 0.24

m-Tyramine (10 μm) and cocaine (0–30 μm) were added at the same time. The data at 0.5, 1, 2, 3, and 4 μm initial [DA]_o were obtained from the same experiments as in Fig. 5. The data at 1.5 μm initial [DA]_o were obtained from other experiments. IC₅₀ was computed by nonlinear fitting the efflux data with logistic equation. All Hill numbers were close to unity (data not shown). For K_i, data were analyzed by the least square linear regression of the v/v′ as a function of the concentrations of an inhibitor.K_i was estimated according to the equation:K_i = 1/{slope of the regression linex (1 + [S]/K_s)}. [S] is the m-tyramine concentration.K_s is the Michaelis–Menten constant form-tyramine to induce DA efflux, and was set at 2.02 μm, which was the average value determined in separate saturation curves (see Table 4). [DA]_o at steady state was measured by RDE voltammetry. [DA]_i was estimated from the linear regression equation expressing the relationship between initial [DA]_o and [DA]_i (see Fig. 1). The values are means ± SE of n experiments.

^F3-aNo significant difference for any [DA] (Newman–Keuls test).