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. Author manuscript; available in PMC: 2011 May 1.
Published in final edited form as: J Neurochem. 2010 Feb 25;113(4):919–929. doi: 10.1111/j.1471-4159.2010.06654.x

Fig. 3.

Fig. 3

The effects of nicotine self-administration (SA) on PVN glutamate (panel a) and GABA release (b) and their incremental or decremental responses (c) induced by mild footshock stress. Glutamate and GABA levels were measured by in vivo microdialysis and HPLC with electrochemical detection, and expressed as a percentage of the pre-footshock baseline levels. Panel (a): Nicotine SA significantly augmented the PVN glutamate response to footshock compared to saline SA (two way ANOVA: time, p < 0.001; SA group, p < 0.01; time × SA group, p < 0.05). Basal glutamate levels for saline vs. nicotine SA: 2331.3 ± 357 vs. 2046.0 ± 510.6 pg/20 μl, respectively (p > 0.05, t-test). *, p < 0.05, vs. 3 pre-shock baseline levels, respectively (t-test); #, p < 0.05, nicotine vs. saline SA at the same time interval, respectively, (t-test). Panel (b): Nicotine SA significantly decreased PVN GABA release in response to footshock compared to saline SA (two way ANOVA: time, p < 0.001; SA group, p < 0.001; time × SA group, p > 0.05). Basal GABA levels for saline vs. nicotine SA: 17.3 ± 1.4 vs 18.4 ± 1.6 pg/20 μl, respectively (p > 0.05, t-test). Panel (c): The cumulative increment in glutamate and decrement in GABA after footshock (across time) were greater in nicotine SA than saline SA groups. , †, p < 0.05, nicotine vs. saline SA, respectively (t-test). All data are expressed as mean ± SEM.