Interplay between glucose and leptin signaling determines the strength of GABAergic synapses at POMC neurons

A) Representative recording samples showing the membrane potential recorded from POMC neurons following treatment with leptin (leptin; 100nM) at 2.5 mM glucose in the absence (left) or presence (right) of the GABA A receptor antagonist picrotoxin (100 M) without glutamatergic influences. Leptin reduced POMC neuronal activity in the absence of the GABA A receptor antagonist, whereas POMC neurons responded to leptin with a depolarization in the presence of the GABA A receptor antagonist. Vm=-48 mV and-55 mV respectively. Scale bar: 20 mV, 2 min. B and C) Graphs showing change in membrane potential (V) from individual POMC neurons before and after treatment with leptin (100 nM) at 2.5 mM glucose (B; left panel, with the glutamate receptor antagonist, n = 38 neurons; right panel, with the glutamate and GABA A receptor antagonists, n = 13 neurons) and 5 mM glucose (C; left panel, with the glutamate receptor antagonist, n = 28 neurons; right panel, with the glutamate and GABA A receptor antagonists, n = 11 neurons). **p < 0.01 vs. control (paired t-test). All data are shown as mean ± SEM.