Skip to main content
. 2012 Nov 14;7(11):e49557. doi: 10.1371/journal.pone.0049557

Figure 2. Ghrelin (into the LDTg) increase VTA-acetylcholine and N.Acc.-dopamine and this involves nicotinic acetylcholine receptors in the VTA.

Figure 2

A) Ghrelin (locally administered into the LDTg at a dose of 1 µg in 0.5 µl) increased ventral tegmental acetylcholine release relative to vehicle treatment. Pre-treatment with the unselective nicotinic acetylcholine receptor antagonist, mecamylamine, locally into the VTA (300 µM) did not affect the ability of ghrelin to increase VTA-acetylcholine. Mecamylamine had no effect on acetylcholine release per se. B) Ghrelin (locally administered into the LDTg at a dose of 1 µg in 0.5 µl) increased accumbal dopamine release relative to vehicle treatment. This increase was attenuated by pre-treatment with the unselective nicotinic acetylcholine receptor antagonist, mecamylamine, locally into the VTA (300 µM). Mecamylamine had no effect on dopamine release per se (n = 10 for vehicle-vehicle (square), n = 11 for vehicle-ghrelin (circle), n = 11 for mecamylamine-vehicle (rhomb), n = 11 for mecamylamine-ghrelin (triangle). All values represent mean ± SEM (***P<0.001, **P<0.01 for vehicle-vehicle versus vehicle-ghrelin and (+++P<0.001, ++P<0.01 for vehicle-vehicle versus mecamylamine-ghrelin).