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

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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, 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.