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First published on January 11, 2005; DOI: 10.1124/mol.104.007427

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Received for publication September 20, 2004.
Revised January 10, 2005.
Accepted for publication January 10, 2005.

Trace amines depress GABAB response in dopaminergic neurons by inhibiting GIRK channels

Mauro Federici 1, Raffaella Geracitano 1, Alessandro Tozzi 1, Patrizia Longone 1, Silvia DiAngelantonio 1, Peter Bengtson 1, Giorgio Bernardi 2, Nicola Biagio Mercuri 3*

1 IRCCS Santa Lucia Foundation, Rome, Italy 2 IRCCS Santa Lucia Foundation; University of Tor Vergata, Rome Italy 3 IRCCS Santa Lucia Foundation; University of Tor Vergata, Rome, Italy

* Address correspondence to: E-mail: mercurin{at}med.uniroma2.it

Abstract

Trace amines (TAs) are present in the central nervous system where they upregulate catecholamine release and are implicated in the pathogenesis of addiction, attention deficit hyperactive 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, {beta}-phenylethylamine ({beta}-PEA) and tyramine (TYR) on the GABAB-mediated slow inhibitory postsynaptic potential (IPSP) and baclofen-activated outward currents. {beta}-PEA and TYR activated G-proteins interfering with the coupling between GABAB receptors and G-{beta}{gamma} gated inwardly rectifying potassium (GIRK) channels. This is the first demonstration that {beta}-PEA and TYR depress inhibitory synaptic potentials in neurons of the central nervous system supporting their emerging role as neuromodulators.


Key words: Dopamine, GABAB, Gi family, cAMP, G protein regulation


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