Figure 3.

Characterization of signalling mechanisms involved in the inhibition of electrically evoked noradrenaline release via mAChRs. Primary cultures of rat SCG neurons were either treated with pertussis toxin (PTX; 100 ng·mL⁻¹ for 24 h) or remained untreated. Cultures were then labelled with [³H]-noradrenaline for 1 h and were 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 10 µmol·L⁻¹ was present as indicated by the arrows; OxoM caused transient increases in the rate of spontaneous ³H outflow (S2) as seen in (A); as a control for statistical comparison, solvent was applied instead of OxoM (see Figure 1A). (A) The time course of fractional ³H outflow·min⁻¹ and its alteration by 10 µmol·L⁻¹ OxoM in untreated (left) or PTX-treated cultures (right); n= 3. (B) ³H overflow induced by 10 µmol·L⁻¹ OxoM (as exemplified by S2% values) in either untreated or PTX-treated cultures; its effect is compared with that of solvent (n= 8 to 9). (C) The inhibition of electrically evoked tritium overflow (as exemplified by S3/S1 ratios) by OxoM; its effect is compared with that of solvent (n= 8 to 9). (D) ³H overflow induced by 10 µmol·L⁻¹ OxoM (as exemplified by S2% values) in either the absence or the presence of 10 µmol·L⁻¹ retigabine; the effect of OxoM is compared with that of solvent (n= 9). (E) The inhibition of electrically evoked tritium overflow by 10 µmol·L⁻¹ OxoM (as exemplified by S3/S1 ratios) in either the absence or the presence of 10 µmol·L⁻¹ retigabine; the effect of OxoM is compared with that of solvent (n= 9). In (B) to (E), significances of differences between pairs of columns are indicated above the corresponding pairs. *** and * Indicate significant differences versus the corresponding results obtained in untreated cultures in the absence of retigabine at P < 0.001 and P < 0.05 respectively; n.s. indicates the lack of such a significance. mAChRs, muscarinic acetylcholine receptors; OxoM, oxotremorine M; PTX, pertussis toxin; SCG, superior cervical ganglia.