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Original Article

Trace Amines Depress GABA_B Response in Dopaminergic Neurons by Inhibiting G--Gated Inwardly Rectifying Potassium Channels

Experimental Neurology Laboratory, S. Lucia Foundation Istituto di Ricovero e Cura a Carattere Scientifico, Rome, Italy; and University of Rome "Tor Vergata", Rome, Italy

Abstract

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, -phenylethylamine (-PEA) and tyramine (TYR) on the GABA_B-mediated slow inhibitory postsynaptic potential and baclofen-activated outward currents. -PEA and TYR activated G-proteins, interfering with the coupling between GABA_B receptors and G--gated inwardly rectifying potassium channels. This is the first demonstration that -PEA and TYR depress inhibitory synaptic potentials in neurons of the central nervous system, supporting their emerging role as neuromodulators.

Received for publication September 20, 2004.

Accepted for publication January 10, 2005.

Address correspondence to: Dr. Nicola Biagio Mercuri, Department of Experimental Neurology, S. Lucia Foundation I.R.C.C.S., Via Ardeatina 306, 00179 Rome, Italy. E-mail: mercurin{at}med.uniroma2.it

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