Figure 4.

H₃R activation attenuates endogenous dopamine exocytosis elicited by depolarization with K⁺ (100 mM) in NGF-differentiated rat pheocromocytoma cells transfected with human H₃R (PC12-H₃). Dopamine exocytosis is inhibited by nifedipine (5 μM), an L-type calcium channel blocker, but not by ω-CTX (100 nM), an N-type calcium channel blocker. The anti-exocytotic effect of imetit (100 nM) is prevented by the H₃R antagonist clobenpropit (CBP; 50 nM), a membrane-permeable phosducin-like anti-βγ peptide (1 μM), and by pre-treatment with PTX (200 ng/ml for 24 hr). Bars are means ± SEM of percent increases in dopamine release above control (n = 18−21). Significantly different from K⁺ alone (*p < 0.05 and **p < 0.01 by ANOVA followed by post hoc Dunnett's test).