A D2 class dopamine receptor transactivates a receptor tyrosine kinase to inhibit NMDA receptor transmission.

Full Abstract

Receptor tyrosine kinases (RTKs) are membrane spanning proteins with intrinsic kinase activity. Although these receptors are known to be involved in proliferation and differentiation of cells, their roles in regulating central synaptic transmission are largely unknown. In CA1 pyramidal neurons, activation of D2 class dopamine receptors depressed excitatory transmission mediated by the NMDA subtype of glutamate receptor. This depression resulted from the quinpirole-induced release of intracellular Ca(2+) and enhanced Ca(2+)-dependent inactivation of NMDA receptors. The dopamine receptor-mediated depression was dependent on the "transactivation" of PDGFRbeta. Therefore, RTK transactivation provides a novel mechanism of communication between dopaminergic and glutamatergic systems and might help to explain how reciprocal changes in these systems could be linked to the deficits in cognition, memory, and attention observed in schizophrenia and attention deficit hyperactivity disorder.

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Author information

Author/s: Kotecha, Suhas A (SA); Oak, James N (JN); Jackson, Michael F (MF); Perez, Yael (Y); Orser, Beverley A (BA); Van Tol, Hubert H M (HH); MacDonald, John F (JF);

Affiliation: Department of Physiology, Faculty of Medicine, University of Toronto, Ontario, Canada.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Neuron (Neuron), published in United States. (Language: eng)

Reference: 2002-Sep; vol 35 (issue 6) : pp 1111-22

Dates: Created 2002/09/30; Completed 2002/10/22; Revised 2006/11/15;

PMID: 12354400, status: MEDLINE (last retrieval date: 11/6/2008)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals
Calcium - metabolism
Calcium Signaling - drug effects; physiology
Calmodulin - metabolism
Cells, Cultured
Dopamine - metabolism; pharmacology
Dopamine Agonists - pharmacology
Dopamine Antagonists - pharmacology
Enzyme Inhibitors - pharmacology
Hippocampus - drug effects; metabolism
Humans

Humans
Pyramidal Cells - drug effects; metabolism
Rats
Rats, Wistar
Receptor Protein-Tyrosine Kinases - drug effects; metabolism
Receptor, Platelet-Derived Growth Factor beta - metabolism
Receptors, Dopamine D2 - drug effects; metabolism
Receptors, N-Methyl-D-Aspartate - drug effects; metabolism
Signal Transduction - drug effects; physiology
Synapses - drug effects; metabolism
Synaptic Transmission - drug effects; physiology

Associated Chemicals: Calmodulin (0) ; Dopamine Agonists (0) ; Dopamine Antagonists (0) ; Enzyme Inhibitors (0) ; Receptors, Dopamine D2 (0) ; Receptors, N-Methyl-D-Aspartate (0) ; Dopamine (51-61-6) ; Calcium (7440-70-2) ; Receptor Protein-Tyrosine Kinases (EC 2.7.1.112) ; Receptor, Platelet-Derived Growth Factor beta (EC 2.7.1.112)

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