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. Author manuscript; available in PMC: 2019 Feb 28.
Published in final edited form as: J Neurochem. 2018 Oct 18;147(2):204–221. doi: 10.1111/jnc.14561

Fig. 3.

Fig. 3

Effects of oxygen-glucose deprivation (OGD) and OGD/R on neuronal glucose uptake (a). Two hours of OGD decreased glucose uptake compared to normoxia which was not statistically significant. However, 24 h reoxygenation following 2-h OGD significantly increased neuronal glucose uptake compared to normoxia and OGD. (b–d) represent effects of short-term (24 h) nicotine (10 μM) and cotinine (5 μM) on neuronal glucose uptake in normoxic, OGD, and OGD/R conditions, respectively: Nicotine and/or cotinine did not cause any significant change in neuronal glucose uptake compared to control both in normoxic and OGD conditions. However, in OGD/R conditions, nicotine and cotinine both caused statistically significant decrease in neuronal glucose uptake compared to control. Combination of nicotine and cotinine resulted in a more significant decrease in glucose uptake compared to control. (e) After long-term (5 days) treatment, nicotine/cotinine also significantly decreased neuronal glucose uptake compared to control in OGD/R conditions. Simultaneous exposure with 20 μM mecamylamine, a non-selective nAChR antagonist, could reverse the effects of nicotine/cotinine treatment on neuronal glucose uptake. Mecamylamine alone did not cause any significant change in neuronal glucose uptake compared to control. N/C, nicotine/cotinine; *p < 0.05, **p < 0.01, ***p < 0.001.