Dopamine–glutamate interactions in the striatum: behaviourally relevant modification of excitotoxicity by dopamine receptor-mediated mechanisms

Garside, Sarah; Furtado, Joarez; Mazurek, Michael F.

doi:10.1016/0306-4522(96)00172-8

Cited by 46 publications

(15 citation statements)

References 62 publications

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“…Localization studies have shown that the D 2 Short receptor is the predominant presynaptic D 2 receptor, whereas D 2 Long is preferentially involved in postsynaptic signaling (Usiello et al, 2000;Lindgren et al, 2003). There is considerable evidence demonstrating that D 2 receptors modulate glutamate-induced neurotoxicity (Garside et al, 1996;Cepeda and Levine, 1998;Sawada et al, 1998). D 2 receptor agonists have shown a protective effect against both hippocampal and nigrostriatal damage after ischemia (Liu et al, 1995;Hall et al, 1996;O'Neill et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Protein-Protein Coupling/Uncoupling Enables Dopamine D₂Receptor Regulation of AMPA Receptor-Mediated Excitotoxicity

Zou

Li²,

Lin³

et al. 2005

J. Neurosci.

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There is considerable evidence that dopamine D 2 receptors can modulate AMPA receptor-mediated neurotoxicity. However, the molecular mechanism underlying this process remains essentially unclear. Here we report that D 2 receptors inhibit AMPA-mediated neurotoxicity through two pathways: the activation of phosphoinositide-3 kinase (PI-3K) and downregulation of AMPA receptor plasma membrane expression, both involving a series of protein-protein coupling/uncoupling events. Agonist stimulation of D 2 receptors promotes the formation of the direct protein-protein interaction between the third intracellular loop of the D 2 receptor and the ATPase N-ethylmaleimide-sensitive factor (NSF) while uncoupling the NSF interaction with the carboxyl tail (CT) of the glutamate receptor GluR2 subunit of AMPA receptors. Previous studies have shown that full-length NSF directly couples to the GluR2 CT and facilitates AMPA receptor plasma membrane expression. Furthermore, the CT region of GluR2 subunit is also responsible for several other intracellular protein couplings, including p85 subunit of PI-3K. Therefore, the direct coupling of D 2 -NSF and concomitant decrease in the NSF-GluR2 interaction results in a decrease of AMPA receptor membrane expression and an increase in the interaction between GluR2 and the p85 and subsequent activation of PI-3K. Disruption of the D 2 -NSF interaction abolished the ability of D 2 receptor to attenuate AMPAmediated neurotoxicity by blocking the D 2 activation-induced changes in PI-3K activity and AMPA receptor plasma membrane expression. Furthermore, the D 2 -NSF-GluR2-p85 interactions are also responsible for the D 2 inhibition of ischemia-induced cell death. These data may provide a new avenue to identify specific targets for therapeutics to modulate glutamate receptor-governed diseases, such as stroke.

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Section: Introductionmentioning

confidence: 99%

Protein-Protein Coupling/Uncoupling Enables Dopamine D₂Receptor Regulation of AMPA Receptor-Mediated Excitotoxicity

Zou

Li²,

Lin³

et al. 2005

J. Neurosci.

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“…For example, KYNA may play a role in the ill-understood neuroprotective effects of hypodopaminergic tone against excitotoxic [Chapman et al, 1989;Filloux and Wamsley, 1991;Garside et al, 1996] and ischemic [Globus et al, 1987] striatal damage, and in the pathophysiology of psychosis [Carlsson and Carlsson, 1990]. KYNA's role in the striatum need not be limited to pathological situations, however, and may extend to the regulation of motor behavior [Graybiel et al, 1994;Kelley and Delfs, 1994].…”

Section: Discussionmentioning

confidence: 99%

“…Notably, dopamine may exacerbate excitotoxicity also by enhancing voltage-sensitive calcium currents [Dugan et al, 1995;Surmeier et al, 1995] and by producing noxious free radicals [Hoyt et al, 1997;Lancelot et al, 1995] which appear to play a critical role in EAA receptor-mediated neuronal injury [Schulz et al, 1995]. In contrast, dopamine depletion or dopamine receptor blockade increases the resistance of striatal neurons to excitotoxic insults [Chapman et al, 1989;Garside et al, 1996].…”

Section: Introductionmentioning

confidence: 99%

Dopaminergic Control of Kynurenate Levels and N-Methyl-<i>D</i>-Aspartate Toxicity in the Developing Rat Striatum

Pöeggeler

Rassoulpour²,

Guidetti³

et al. 1998

Dev Neurosci

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This study was designed to examine the effects of d-amphetamine (D-AMPH) and D1- and D2-selective dopaminergic drugs on the concentration of the broad-spectrum excitatory amino acid receptor antagonist kynurenic acid (KYNA) in the striatum of developing and adult rats. At all ages, KYNA levels were significantly reduced 1 h after the systemic administration of D-AMPH (5 mg/kg). SKF 38393 (5 mg/kg) and quinpirole (2 mg/kg) also caused a rapid decrease in striatal KYNA, but only in postnatal day (PND) 7 and 14 rats. All these effects were readily prevented by specific dopamine receptor antagonists. The possible functional significance of the reduction in KYNA levels was tested in PND 14 animals. When pretreated with D-AMPH (5 mg/kg), these rats showed markedly increased vulnerability to an intrastriatal injection of the excitotoxin NMDA. These data suggest that KYNA plays a role as a mediator of dopamine-glutamate interactions in the rat striatum.

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“…Several lines of evidence have recently indicated that the interactions between different neurotransmitter systems are of great significance in regulating brain functions. Interaction between dopaminergic and glutamatergic systems has been suggested to be involved in the regulation of psychomotor functions (Amalric et al, 1994;Carlsson and Carlsson, 1990;Garside et al, 1996;Keefe et al, 1993;Loscher and Honack, 1992;Pralong and Jones, 1993;Wu et al, 1993). In addition, several reports have shown that the serotonergic system, along with dopamine-glutamate interaction, plays an important role in behavior, learning, arachidonic acid turnover, and other higher brain functions (French and Ceci, 1990;Meneses and Hong, 1997;Ohta et al, 1994;Rinne et al, 1995;Schmidt and Fadayel, 1996;Strosznajder et al, 1994 (Kobayashi and Inoue, 1993), and the in vivo binding characteristics of [ 123 I]␤-CIT in rat brain have been shown to be significantly altered by the 5HT transporter inhibitor clomipramine (Fujita et al, 1997).…”

Section: ␤-Citmentioning

confidence: 99%

Enhancement of in vivo binding of [123I]?-CIT by MK-801 in rat brain

Nakano

Takatoku

Matoba

et al. 1998

Synapse

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The effects of MK-801, a noncompetitive NMDA receptor antagonist, on in vivo and in vitro binding of radioactive iodine ([123I] or [125I]) labeled beta-CIT [RTI-55, 3beta-(4-iodophenyl)tropane-2beta-carboxylic acid methyl ester] were investigated in rat brain. In the in vitro binding study, 10 pM of [125I]beta-CIT was incubated with either 0.03 microM or 3 microM of MK-801 at 24 degrees C for 60 min. In vitro, no alterations in [125I]beta-CIT binding in any region of rat brain slices were detected after addition of MK-801. In the in vivo binding study, [123I]beta-CIT was intravenously injected into rats 30 min after intraperitoneal injection of 0.03-1 mg/kg of MK-801. The in vivo [123I]beta-CIT binding in the striatum, frontal cortex, occipital cortex, hypothalamus, and thalamus was significantly increased by pretreatment with 1 mg/kg of MK-801. Kinetic analysis using the cerebellum as a reference region revealed that the increases in in vivo [123I]beta-CIT binding induced by MK-801 were mainly due to increases in both input rate constant k3 and output rate constant k4. The results of this study indicate that the glutamatergic system, including NMDA receptor, plays an important role in regulating neurotransmission in the dopaminergic or serotonergic systems in intact brain.

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Dopamine–glutamate interactions in the striatum: behaviourally relevant modification of excitotoxicity by dopamine receptor-mediated mechanisms

Cited by 46 publications

References 62 publications

Protein-Protein Coupling/Uncoupling Enables Dopamine D₂Receptor Regulation of AMPA Receptor-Mediated Excitotoxicity

Protein-Protein Coupling/Uncoupling Enables Dopamine D₂Receptor Regulation of AMPA Receptor-Mediated Excitotoxicity

Dopaminergic Control of Kynurenate Levels and N-Methyl-<i>D</i>-Aspartate Toxicity in the Developing Rat Striatum

Enhancement of in vivo binding of [123I]?-CIT by MK-801 in rat brain

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Dopamine–glutamate interactions in the striatum: behaviourally relevant modification of excitotoxicity by dopamine receptor-mediated mechanisms

Cited by 46 publications

References 62 publications

Protein-Protein Coupling/Uncoupling Enables Dopamine D2Receptor Regulation of AMPA Receptor-Mediated Excitotoxicity

Protein-Protein Coupling/Uncoupling Enables Dopamine D2Receptor Regulation of AMPA Receptor-Mediated Excitotoxicity

Dopaminergic Control of Kynurenate Levels and N-Methyl-<i>D</i>-Aspartate Toxicity in the Developing Rat Striatum

Enhancement of in vivo binding of [123I]?-CIT by MK-801 in rat brain

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Protein-Protein Coupling/Uncoupling Enables Dopamine D₂Receptor Regulation of AMPA Receptor-Mediated Excitotoxicity

Protein-Protein Coupling/Uncoupling Enables Dopamine D₂Receptor Regulation of AMPA Receptor-Mediated Excitotoxicity