PT  - JOURNAL ARTICLE
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
TI  - Trace Amines Depress GABA<sub>B</sub> Response in Dopaminergic Neurons by Inhibiting G-βγ-Gated Inwardly Rectifying Potassium Channels
AID  - 10.1124/mol.104.007427
DP  - 2005 Apr 01
TA  - Molecular Pharmacology
PG  - 1283--1290
VI  - 67
IP  - 4
4099  - http://molpharm.aspetjournals.org/content/67/4/1283.short
4100  - http://molpharm.aspetjournals.org/content/67/4/1283.full
SO  - Mol Pharmacol2005 Apr 01; 67
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.