Abstract
Trace amines (TAs) act in the mammalian brain through amphetamine-like effects and as endogenous agonists of specific receptors. We now show that tyramine and beta-phenylethylamine, in the presence of specific dopamine (DA) receptor antagonists, inhibit the GABA(B)-dependent presynaptic inhibition of GABAergic inputs to midbrain DA neurons. Our results further extend the role of TAs as neuromodulators and propose a novel mechanism by which they modulate DA neurons.
MeSH terms
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Animals
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Biogenic Monoamines / metabolism*
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Dopamine / metabolism
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GABA Agonists / metabolism
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Neural Inhibition / physiology*
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Neurotransmitter Agents / metabolism*
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Organ Culture Techniques
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Patch-Clamp Techniques
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Presynaptic Terminals / metabolism
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Rats
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Rats, Wistar
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Receptors, GABA-B / metabolism*
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Statistics, Nonparametric
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Substantia Nigra / cytology
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Substantia Nigra / metabolism*
Substances
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Biogenic Monoamines
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GABA Agonists
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Neurotransmitter Agents
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Receptors, GABA-B
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Dopamine