RT Journal Article SR Electronic T1 Trace Amines Depress GABAB Response in Dopaminergic Neurons by Inhibiting G-βγ-Gated Inwardly Rectifying Potassium Channels JF Molecular Pharmacology JO Mol Pharmacol FD American Society for Pharmacology and Experimental Therapeutics SP 1283 OP 1290 DO 10.1124/mol.104.007427 VO 67 IS 4 A1 Mauro Federici A1 Raffaella Geracitano A1 Alessandro Tozzi A1 Patrizia Longone A1 Silvia Di Angelantonio A1 C. Peter Bengtson A1 Giorgio Bernardi A1 Nicola B. Mercuri YR 2005 UL http://molpharm.aspetjournals.org/content/67/4/1283.abstract AB 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.