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39 �� 13.01% (n= 7), 17.25 �� 3.95% (n= 6) and 4.52 �� 3.26% (n= 6), respectively (Fig. 2E). In perforated mode, the open probability of KATP channels measured with the approach described above was 0.3 �� 0.36% (n= 4), suggesting that the KATP channels are in the closed state in Hcrt neurones with intact intracellular http://en.wikipedia.org/wiki/Diglyceride ATP levels. In summary, these results suggest that [ATP]i has a profound effect on the opening of KATP channels in Hcrt neurones, which may significantly dictate the Vm in these cells. Next, we tested whether the interruption of ATP production by blocking oxidative phosphorylation or decreasing extracellular glucose has any effects on Vm in Hcrt neurones. In perforated mode, the application of NaN3 (1 mm, an inhibitor of oxidative phosphorylation) through ACSF (Matsumoto et al. 2002) significantly hyperpolarized Hcrt neurones a few minutes later (control: ?50.0 �� 1.4 mV, n= 9; NaN3: ?63.7 �� 1.2 mV, n= 9; washout: ?48.9 �� 1.4 mV, n= 9; P http://www.selleckchem.com/products/AZD0530.html of NaN3 did not induce any changes in Vm in this protocol (control: ?47.4 �� 2.0 mV, n= 5; NaN3: ?47.7 �� 2.1 mV, n= 5; washout: ?45.3 �� 1.7 mV, n= 5, P > 0.05, ANOVA, Fig. 3E and F). In a parallel set of experiments, we lowered the extracellular glucose concentration from 2.5 mm to 0.1 mm in the ACSF. The Vm of Hcrt neurones did not exhibit an acute change in response to the initial decrease in extracellular glucose concentration, but rather significantly hyperpolarized about 20 min later (control: ?48.41 �� 1.66 mV, n= 7; low glucose: ?53.46 �� 1.73 mV, n= 7, washout: ?45.07 �� 1.81 mV, P http://www.selleckchem.com/products/GDC-0941.html + tolbutamide: ?46.63 �� 1.44 mV, n= 7, P