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. 2023 Aug 2;76:101788. doi: 10.1016/j.molmet.2023.101788

Figure 1.

Figure 1

Glucose sensing in hcrt/ox-GI neurons is mediated by protein kinase A (PKA). A. Representative whole cell voltage clamp recording of a hcrt/ox-GI neuron. When extracellular glucose decreased from 2.5 to 0.1 mM, this neuron reversibly depolarized its membrane potential (MP) and increased whole cell resistance (R) and action potential frequency. R was calculated by measuring the voltage response (downward deflection, expanded in inset to the right) to a constant hyperpolarizing current pulse (Ohm's Law: voltage (V) = current (I) x R). B–C. Percent change in MP and R in response to decreased glucose from 2.5 to 0.1 in the presence and absence (control) of: (B) the G-protein coupled receptor blocker, pertussis toxin (PTX, 500 ng/ml); brain slices were incubated in PTX for 2 h prior to recording (control, n/N (# neurons/#mice) = 6/4; PTX, n/N = 11/11, Independent Student's t-test) and (C) the PKA inhibitor, Rp-cAMP (10 μM; Rp) added to the bath solution (n/N = 5/5, Paired Student's t-test).∗∗∗P < 0.001, ∗∗∗∗P < 0.0001. D. Representative voltage responses to decreased glucose in the presence and absence of Rp-cAMP (gray: 2.5, black 0.1 mM glucose). Data represented as mean ± SEM.