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. Author manuscript; available in PMC: 2015 Apr 1.

Published in final edited form as: J Neurochem. 2013 Nov 25;129(1):48–59. doi: 10.1111/jnc.12527

Each experiment was repeated 3 times.

4a: Human CHGB protein or its proteolytically-digested fragments on nicotinic cholinergic versus membrane depolarization (KCl) -stimulated catecholamine release. CHGB protein or its plasmin-digested fragments inhibited predominantly nicotine-stimulated catecholamine release. 4b: Left: Synthetic CHGB peptides on nicotinic cholinergic stimulated catecholamine release. Catestatin (human CHGA[352–372]) served as a positive inhibitory control. Peptide human CHGB[60–67] displayed the greatest inhibitory effect among these peptides. P value is displayed for each peptide compared with negative control. Middle: Synthesized Human CHGB peptides on membrane depolarization (KCl)- stimulated catecholamine release. Catestatin (human CHGA[352–372]) served as a positive inhibitory control. No inhibitory effect was observed for these peptides (p>0.05 for each peptide).

Right: Potency and efficacy of CHGB[60–67] on nicotinic cholinergic-stimulated catechalmine release. Catestatin (human CHGA[352–372]) served as a positive control. Potency and efficacy of CHGB[60–67] are displayed. 4c: CHGB peptide effect on nicotinic cholinergic cationic (Ca²⁺) signal transduction in chromaffin cells. PC12 cells were treated with ⁴⁵Ca²⁺ at 2 µCi/ml and incubated under different conditions including basal, nicotine alone at 60 µM, and nicotine with hCHGA or hCHGB peptides. Catestatin (human CHGA[352–372]) served as a positive control inhibitor. Human CHGB[60–67] moderately (by ~22%) inhibited nicotine-triggered uptake of ⁴⁵Ca.

Each experiment was repeated 3 times.

4a: Human CHGB protein or its proteolytically-digested fragments on nicotinic cholinergic versus membrane depolarization (KCl) -stimulated catecholamine release. CHGB protein or its plasmin-digested fragments inhibited predominantly nicotine-stimulated catecholamine release. 4b: Left: Synthetic CHGB peptides on nicotinic cholinergic stimulated catecholamine release. Catestatin (human CHGA[352–372]) served as a positive inhibitory control. Peptide human CHGB[60–67] displayed the greatest inhibitory effect among these peptides. P value is displayed for each peptide compared with negative control. Middle: Synthesized Human CHGB peptides on membrane depolarization (KCl)- stimulated catecholamine release. Catestatin (human CHGA[352–372]) served as a positive inhibitory control. No inhibitory effect was observed for these peptides (p>0.05 for each peptide).

Right: Potency and efficacy of CHGB[60–67] on nicotinic cholinergic-stimulated catechalmine release. Catestatin (human CHGA[352–372]) served as a positive control. Potency and efficacy of CHGB[60–67] are displayed. 4c: CHGB peptide effect on nicotinic cholinergic cationic (Ca²⁺) signal transduction in chromaffin cells. PC12 cells were treated with ⁴⁵Ca²⁺ at 2 µCi/ml and incubated under different conditions including basal, nicotine alone at 60 µM, and nicotine with hCHGA or hCHGB peptides. Catestatin (human CHGA[352–372]) served as a positive control inhibitor. Human CHGB[60–67] moderately (by ~22%) inhibited nicotine-triggered uptake of ⁴⁵Ca.