Abstract
Evidence has been presented that behavioral actions of NT, inducing its neuroleptic-like action, can be explained on the basis of NT-D2 intramembrane receptor-receptor interactions in the basal ganglia, unrelated to the coexistence phenomenon, leading to reduced affinity and transduction of the D2 agonist binding site. By reducing selectively D2 receptor transduction at the pre- and postsynaptic level, the NT receptor appears capable of switching the DA synapses towards a D1 receptor-mediated transduction, illustrating how receptor-receptor interactions can increase the functional plasticity of central synapses (FIG. 12).
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Antipsychotic Agents / metabolism*
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Apomorphine / analogs & derivatives
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Apomorphine / metabolism
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Basal Ganglia / metabolism
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Behavior, Animal / drug effects
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Brain / metabolism*
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Cell Membrane / metabolism
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Dopamine / metabolism
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Dopamine / pharmacology
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Dopamine Agents / metabolism
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Enkephalins / metabolism
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GTP-Binding Proteins / metabolism
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Neurons / chemistry
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Neurotensin / metabolism*
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Neurotensin / pharmacology
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Oxidopamine / pharmacology
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Rats
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Receptors, Dopamine D2 / metabolism*
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Receptors, Neurotensin
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Receptors, Neurotransmitter / metabolism*
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gamma-Aminobutyric Acid / metabolism
Substances
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Antipsychotic Agents
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Dopamine Agents
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Enkephalins
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Receptors, Dopamine D2
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Receptors, Neurotensin
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Receptors, Neurotransmitter
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Neurotensin
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gamma-Aminobutyric Acid
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N-n-propylnorapomorphine
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Oxidopamine
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GTP-Binding Proteins
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Apomorphine
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Dopamine