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. Author manuscript; available in PMC: 2015 Jul 28.
Published in final edited form as: Neuropharmacology. 2009 Dec 22;58(6):921–929. doi: 10.1016/j.neuropharm.2009.12.005

Fig. 2.

Fig. 2

Agonist-induced regulation of cell proliferation is blocked by receptor-selective antagonists indicating positive regulation mediated by the muscarinic M1 receptor. a, BrdU+ cell counts in the DG and CA1 regions of the hippocampus following oxotremorine. Chronic intraventricular administration of the M1 receptor antagonist, pirenzepine, but not the nicotinic antagonist, mecamylamine, dose-dependently blocked oxotremorine-induced elevations in BrdU immunolabeling in both the DG and CA1. b, Chronic intraventricular administration of the M1 receptor antagonist, pirenzepine, also dose-dependently blocked low dose carbachol-induced elevations in BrdU immunolabeling. By contrast, the nicotinic receptor antagonist, mecamylamine, had no effect. As described earlier, a higher dose of carbachol (30 μg/h) failed to affect cell proliferation. Co-administration with mecamylamine, however, dose-dependently elevated BrdU immunolabeling while co-administration with pirenzepine significantly reduced BrdU immunolabeling. Each bar represents the mean (±S.E.M.) (n = 6) number of BrdU+ cells per mm3. ** sig. diff. from saline-treated controls, p < 0.001, *p < 0.05; ++ sig. diff. from oxotremorine alone, p < 0.001, +p < 0.05.