Figure 1.

Enhancement of spontaneous and inhibition of electrically evoked noradrenaline release by OxoM via different sets of receptors. Primary cultures of rat SCG neurons were labelled with [³H]-noradrenaline for 1 h and then superfused. Subsequent to a 60 min washout period, 4 min fractions of superfusate were collected. Electrical field stimulation was applied at 73 (S1) and 113 (S3) min of superfusion. OxoM, either alone or together with pirenzepine or methoctramine, was present as indicated by the arrow on the right hand side in (A) and caused transient increases in the rate of spontaneous ³H outflow (S2); as a control for statistical comparison, solvent was applied instead of OxoM. (A) The time course of fractional ³H outflow·min⁻¹ and its alteration by 10 µmol·L⁻¹ OxoM on the right hand side (n= 3). For comparison, the effect of solvent is depicted on the left hand side (n= 3). (B) The concentration-dependence of OxoM-induced ³H overflow, as exemplified by S2% values. The indicated concentrations of OxoM were applied as shown in (A) (n= 5 to 6). (C) The concentration-dependence of the inhibition of electrically evoked tritium overflow by OxoM, as exemplified by S3/S1 ratios. The indicated concentrations of OxoM were applied as shown in (A) (n= 5 to 6). (D) The concentration-dependent attenuation of the ³H overflow induced by 10 µmol·L⁻¹ OxoM by pirenzepine or methoctramine, as exemplified by S2% values. OxoM (10 µmol·L⁻¹) was applied as shown in (A) either alone or together with the indicated concentrations of pirenzepine or methoctramine (n= 6 to 8). (E) The concentration-dependent attenuation of the inhibition of electrically evoked tritium overflow by 10 µmol·L⁻¹ OxoM in the presence of pirenzepine or methoctramine, as exemplified by S3/S1 ratios. OxoM (10 µmol·L⁻¹) was applied as shown in (A) either alone or together with the indicated concentrations of pirenzepine or methoctramine (n= 6 to 8). OxoM, oxotremorine M; SCG, superior cervical ganglia.