Interaction of dopamine D1 with NMDA NR1 receptors in rat prefrontal cortex

Kruse, María Sol; Prémont, Joël; Krebs, Marie‐Odile; Jay, Thérèse M.

doi:10.1016/j.euroneuro.2008.12.006

Cited by 52 publications

(32 citation statements)

References 41 publications

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“…In addition, the D1-NMDA receptor complex may be of relevance for disorders involving cognitive dysfunction such as schizophrenia, as activation of the D1R upregulated NMDA receptor-mediated LTP in hippocampus in a CaMKIIdependent manner and promoted working memory, whereas uncoupling the D1-NMDA complex abolished the D1R-induced upregulation of NMDA-mediated LTP and impaired working memory in mice (Nai et al, 2010). Interestingly, an interaction between the D1R and NMDA receptor was also demonstrated in rat PFC (Kruse et al, 2009), a region critically involved in the cognitive impairments inherent in schizophrenia (Lewis, 2012), and in which NMDA hypofunction has been implicated (Jentsch et al, 1997;Mohn et al, 1999). It has thus been suggested that reduced D1R and NMDA function may contribute to the etiology of schizophrenia, and additionally, that the prefrontal cortical hypodopaminergia inherent in the disorder may be secondary to NMDA receptor dysfunction (Nai et al, 2010).…”

Section: Dopamine-nmda Receptor Heteromers: D1-nr1 D2-nr2bmentioning

confidence: 91%

Heteromeric Dopamine Receptor Signaling Complexes: Emerging Neurobiology and Disease Relevance

Perreault

Hasbi

O’Dowd

et al. 2013

Neuropsychopharmacol

134

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The pharmacological modification of dopamine transmission has long been employed as a therapeutic tool in the treatment of many mental health disorders. However, as many of the pharmacotherapies today are not without significant side effects, or they alleviate only a particular subset of symptoms, the identification of novel therapeutic targets is imperative. In light of these challenges, the recognition that dopamine receptors can form heteromers has significantly expanded the range of physiologically relevant signaling complexes as well as potential drug targets. Furthermore, as the physiology and disease relevance of these receptor heteromers is further understood, their ability to exhibit pharmacological and functional properties distinct from their constituent receptors, or modulate the function of endogenous homomeric receptor complexes, may allow for the development of alternate therapeutic strategies and provide new avenues for drug design. In this review, we describe the emerging neurobiology of the known dopamine receptor heteromers, their physiological relevance in brain, and discuss the potential role of these receptor complexes in neuropsychiatric disease. We highlight their value as targets for future drug development and discuss innovative research strategies designed to selectively target these dopamine receptor heteromers in the search for novel and clinically efficacious pharmacotherapies.

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Section: Dopamine-nmda Receptor Heteromers: D1-nr1 D2-nr2bmentioning

confidence: 91%

Heteromeric Dopamine Receptor Signaling Complexes: Emerging Neurobiology and Disease Relevance

Perreault

Hasbi

O’Dowd

et al. 2013

Neuropsychopharmacol

134

View full text Add to dashboard Cite

show abstract

“…Scale bar, 50 m. inducing expression of immediate-early genes, including Egr1 and arc, which play a crucial role in reference memory (Guzowski et al, 2000;Jones et al, 2001). Alternatively, D 1 Rs could directly phosphorylate NMDA receptors or the protein kinase C isoform in hippocampus and amygdala, potentiating and maintaining synaptic strength (Gardner et al, 2001;Impey et al, 2002;Kelleher et al, 2004;Sacktor, 2008;Yao et al, 2008) by increasing the influx of calcium induced by NMDA receptor activation, as occurs in prefrontal cortex neurons (Kruse et al, 2009). Direct interaction between D 1 and NMDA receptors within the plasma membrane of pyramidal neurons may also occur, since D 1 R can physically interact with NR1 and NR2A subunits, modulating receptor trafficking (Lee et al, 2002;Pei et al, 2004;Fiorentini et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Associative Learning and CA3–CA1 Synaptic Plasticity Are Impaired in D₁R Null,Drd1a^−/−Mice and in Hippocampal siRNA SilencedDrd1aMice

Ortiz¹,

Delgado‐García²,

Espadas³

et al. 2010

J. Neurosci.

128

120

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Associative learning depends on multiple cortical and subcortical structures, including striatum, hippocampus, and amygdala. Both glutamatergic and dopaminergic neurotransmitter systems have been implicated in learning and memory consolidation. While the role of glutamate is well established, the role of dopamine and its receptors in these processes is less clear. In this study, we used two models of dopamine D 1 receptor (D 1 R, Drd1a) loss, D 1 R knock-out mice (Drd1a

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“…Importantly, dopamine receptor and NMDA receptor activities functionally converge through both direct physical association and the activation of cell signaling pathways [24,[73][74][75][76][77] . One of the molecular connections between dopamine receptor and NMDA receptor activity in striatal neurons is the phosphorylation of NR1 at Ser897 [78] , a modification that was recently shown to be increased by NMDA and which is oppositely regulated by D1 and D3 receptor activity [19] .…”

Section: Discussionmentioning

confidence: 99%

Signaling via Dopamine D1 and D3 Receptors Oppositely Regulates Cocaine-Induced Structural Remodeling of Dendrites and Spines

Zhang

Li²,

Liu³

et al. 2011

Neurosignals

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Repeated exposure to cocaine can induce persistent alterations in the brain. The structural remodeling of dendrites and dendritic spines is thought to play a critical role in cocaine addiction. We previously demonstrated that signaling via dopamine D1 and D3 receptors have opposite effects on cocaine-induced gene expression. Here, we show that cocaine-induced structural remodeling in the nucleus accumbens (NAc) and caudoputamen (CPu) is mediated by D1 receptors and inhibited by D3 receptors. In addition, chronic exposure to cocaine results in an altered number of asymmetric spine synapses via the actions of both D1 and D3 receptors. The contradictory effects of D1 and D3 receptor signaling on cocaine-induced structural remodeling is associated with NMDA-receptor R1 subunit (NR1) phosphorylation, and is dependent upon the activation of extracellular signal-regulated kinase (ERK). In addition, we found that D1 and D3 receptor signaling has contradictory effects upon the activation of the myocyte enhancer factor 2 (MEF2), which is involved in the dendritic remodeling after cocaine treatment. Together, these data suggest that dopamine D1 and D3 receptors differentially regulate the cocaine-induced structural remodeling of dendrites and spines via mechanisms involving the consecutive actions of NR1 phosphorylation, ERK activation, and MEF2 activity in the NAc and CPu.

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Interaction of dopamine D1 with NMDA NR1 receptors in rat prefrontal cortex

Cited by 52 publications

References 41 publications

Heteromeric Dopamine Receptor Signaling Complexes: Emerging Neurobiology and Disease Relevance

Heteromeric Dopamine Receptor Signaling Complexes: Emerging Neurobiology and Disease Relevance

Associative Learning and CA3–CA1 Synaptic Plasticity Are Impaired in D₁R Null,Drd1a^−/−Mice and in Hippocampal siRNA SilencedDrd1aMice

Signaling via Dopamine D1 and D3 Receptors Oppositely Regulates Cocaine-Induced Structural Remodeling of Dendrites and Spines

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Interaction of dopamine D1 with NMDA NR1 receptors in rat prefrontal cortex

Cited by 52 publications

References 41 publications

Heteromeric Dopamine Receptor Signaling Complexes: Emerging Neurobiology and Disease Relevance

Heteromeric Dopamine Receptor Signaling Complexes: Emerging Neurobiology and Disease Relevance

Associative Learning and CA3–CA1 Synaptic Plasticity Are Impaired in D1R Null,Drd1a−/−Mice and in Hippocampal siRNA SilencedDrd1aMice

Signaling via Dopamine D1 and D3 Receptors Oppositely Regulates Cocaine-Induced Structural Remodeling of Dendrites and Spines

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Product

Resources

About

Associative Learning and CA3–CA1 Synaptic Plasticity Are Impaired in D₁R Null,Drd1a^−/−Mice and in Hippocampal siRNA SilencedDrd1aMice