Dopamine and N-methyl-D-aspartate receptor interactions in the neostriatum.
This review examines dopamine (DA) and glutamate receptor interactions in the neostriatum (NS) primarily from a neurophysiological perspective. Historically, a clear understanding of the function of DA in the NS has been difficult because it was considered a classical neurotransmitter with either excitatory or inhibitory actions and because many of the data were obtained by use of varying methodologies. When DA is considered a neuromodulator whose role is to alter how NS cells respond to glutamatergic inputs, many of its actions can be accounted for and predicted with great accuracy within a model of receptor subtype. In this model, DA via activation of D1 receptors potentiates responses mediated by activation of N-methyl-D-aspartate (NMDA) receptors. DA via activation of D2 receptors attenuates responses mediated by activation of non-NMDA receptors. Outcomes of combinations of NMDA and D2 and non-NMDA and D1 receptors are not as predictable. The mechanisms underlying the D1-NMDA receptor interactions appear to involve alterations in cell excitability mediated by activation of Ca2+ conductances and/or phosphorylation of NMDA receptors. Less is known about mechanisms underlying the D2-non-NMDA receptor interaction. The functional implications of this model in setting membrane potentials, signal-to-noise ratio, plasticity and excitotoxicity are discussed.
Cepeda
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Mental Retardation Research Center, University of California at Los Angeles, 90024-1759, USA.
Levine
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MS
D000344:Afferent Pathways / Q000502:physiology; D000375:Aging / Q000502:physiology; D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000502:physiology; D020746:Calcium Channels, L-Type; D002540:Cerebral Cortex / Q000502:physiology; D000242:Cyclic AMP / Q000502:physiology; D004298:Dopamine / Q000502:physiology*; D015259:Dopamine Agents / Q000494:pharmacology; D005314:Embryonic and Fetal Development / Q000502:physiology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000502:physiology*; D006801:Humans; D017136:Ion Transport / Q000187:drug effects; D008959:Models, Neurological; D017072:Neostriatum / Q000502:physiology*; D009419:Nerve Tissue Proteins / Q000502:physiology*; D009473:Neuronal Plasticity / Q000187:drug effects; D009474:Neurons / Q000145:classification / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D011954:Receptors, Dopamine / Q000145:classification / Q000187:drug effects / Q000502:physiology*; D017470:Receptors, Glutamate / Q000145:classification / Q000187:drug effects / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects / Q000502:physiology*; D015398:Signal Transduction / Q000187:drug effects; D013378:Substantia Nigra / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects
D015220:Calcium Channels; D020746:Calcium Channels, L-Type; D015259:Dopamine Agents; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D009419:Nerve Tissue Proteins; D011954:Receptors, Dopamine; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D000242:Cyclic AMP; D002118:Calcium; D004298:Dopamine