TY - JOUR T1 - Trace Amines Depress GABA<sub>B</sub> Response in Dopaminergic Neurons by Inhibiting G-βγ-Gated Inwardly Rectifying Potassium Channels JF - Molecular Pharmacology JO - Mol Pharmacol SP - 1283 LP - 1290 DO - 10.1124/mol.104.007427 VL - 67 IS - 4 AU - Mauro Federici AU - Raffaella Geracitano AU - Alessandro Tozzi AU - Patrizia Longone AU - Silvia Di Angelantonio AU - C. Peter Bengtson AU - Giorgio Bernardi AU - Nicola B. Mercuri Y1 - 2005/04/01 UR - http://molpharm.aspetjournals.org/content/67/4/1283.abstract N2 - Trace amines (TAs) are present in the central nervous system in which they up-regulate catecholamine release and are implicated in the pathogenesis of addiction, attention-deficit/hyper-activity disorder, Parkinson's disease, and schizophrenia. By using intracellular and patch-clamp recordings from dopaminergic cells in the rat midbrain slices, we report a depressant postsynaptic action of two TAs, β-phenylethylamine (β-PEA) and tyramine (TYR) on the GABAB-mediated slow inhibitory postsynaptic potential and baclofen-activated outward currents. β-PEA and TYR activated G-proteins, interfering with the coupling between GABAB receptors and G-βγ-gated inwardly rectifying potassium channels. This is the first demonstration that β-PEA and TYR depress inhibitory synaptic potentials in neurons of the central nervous system, supporting their emerging role as neuromodulators. ER -