Objective: Glucagon-like-peptide 1 (GLP-1) injected into the brain causes satiety. Neurons that express preproglucagon (PPG) make GLP-1 and are found in nucleus tractus solitarius (NTS). In order to analyze functional properties of PPG neurons we used transgenic mice expressing YFP under PPG promoter control, thus allowing patch- clamp recordings from PPG cells identified by fluorescence. Hindbrain catecholaminergic neurons have been implicated in glucoprivic feeding. Here we investigated whether these cells impinge on PPG neurons by analyzing the effect of catecholamines on PPG neurons. Methods: Slices were obtained from adult transgenic mice after halothane anaesthesia. Perforated patch-clamp (current clamp) and conventional whole-cell (voltage clamp) recordings were performed on PPG neurons under visual control at 32°C. Results: In current-clamp, 10 mM adrenaline (AD) and 100 mM noradrenaline (NA) increased action potential firing rate (1.5±0.3 to 2.3±0.5 Hz, 1.4±0.3 to 2.7±0.5 Hz, respectively), but had no effect on membrane potential and conductance. In voltage-clamp, AD and NA increased the frequency of spontaneous excitatory synaptic currents (sEPSCs). Kynurenic acid reduced the frequency of sEPSCs from 2.4±0.5 Hz to 0.2±0.04 Hz and blocked the AD-induced increase in sEPSC frequency (n=5). The AD effect was also prevented by the 2 receptor antagonist yohimbine (n=5). TTX reduced sEPSC frequency from 3.0±0.6 Hz to 0.7±0.1 Hz in 15 out of 24 PPG cells and blocked the effect of AD. In the remaining 9 PPG neurons TTX did not affect sEPSC frequency and the AD effect remained in 5 of these cells. Conclusion: PPG neurons do not receive a direct adrenergic input, but their glutamatergic input is modulated by a2-adrenergic receptor activation. This modulation takes place at either of two sites: at the glutamatergic synapse (TTX- resistant) or distant from the synapse (TTX- sensitive).