Ca2+-permeable AMPA (α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid) Receptors and Dopamine D1 Receptors Regulate GluA1 Trafficking in Striatal Neurons

Tukey, David S.; Ziff, Edward B.

doi:10.1074/jbc.m113.516690

Cited by 19 publications

(11 citation statements)

References 63 publications

(59 reference statements)

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“…AMPARs are co-expressed with DA receptors in NAc neurons [30], and most are either GluA1/GluA2 or GluA2/GluA3 heteromers [31]. GluA2-lacking AMPA receptors make up only 5–10% of the total but, when present, are of note because they increase Ca 2+ conductance and enable Ca 2+ -dependent intracellular signaling which can traffic additional GluA1-containing AMPARs to the synaptic membrane [32] and mediate synaptic strengthening via long term potentiation [33,34]. …”

Section: Effects Of Sucrose and Food Restriction On Ampa Receptor Phomentioning

confidence: 99%

“…This set of events is similar to those occurring in homeostatic synaptic scaling, where CP-AMPARs are inserted into the synaptic membrane following prolonged neuronal deprivation of excitatory input and decreased intracellular Ca 2+ signaling [46,47]. A homeostatic incorporation of CP-AMPARs in NAc of FR rats could account, at least in part, for increased D-1 receptor dependent neuronal excitation and downstream behavioral effects, as well as the increased stimulus-induced trafficking of additional GluA1-containing AMPARs (GluA1 or GluA1/GluA2) to the postsynapse [32–34]. …”

Section: Food Restriction Induces Synaptic Incorporation Of Calcium-pmentioning

confidence: 99%

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Nucleus accumbens AMPA receptor trafficking upregulated by food restriction: an unintended target for drugs of abuse and forbidden foods

Carr

2016

Current Opinion in Behavioral Sciences

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There is a high rate of comorbidity between eating disorders and substance abuse, and specific evidence that weight-loss dieting can increase risk for binge pathology, rebound excessive weight gain, and initiation and relapse to drug abuse. The present overview discusses basic science findings indicating that chronic food restriction induces dopamine conservation, compensatory upregulation of D-1 dopamine receptor signaling, and synaptic incorporation of calcium-permeable glutamatergic AMPA receptors in nucleus accumbens. Evidence is presented which indicates that these neuroadaptations account for increased incentive effects of food, drugs, and associated environments during food restriction. In addition, these same neuroadaptations underlie upregulation of sucrose- and psychostimulant-induced trafficking of AMPA receptors to the nucleus accumbens postsynaptic density, which may be a mechanistic basis of enduring maladaptive behavior.

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Section: Effects Of Sucrose and Food Restriction On Ampa Receptor Phomentioning

confidence: 99%

Section: Food Restriction Induces Synaptic Incorporation Of Calcium-pmentioning

confidence: 99%

Nucleus accumbens AMPA receptor trafficking upregulated by food restriction: an unintended target for drugs of abuse and forbidden foods

Carr

2016

Current Opinion in Behavioral Sciences

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“…It is well-established that NMDA receptors are both coupled to and regulated by nitric oxide signaling, facilitated by the synaptic scaffold protein PSD-95, which bridges NMDA receptor-associated Ca 2+ channels with neuronal nitric oxide synthase (nNOS) [ 24 , 44 ]. In addition, both colocalization and functional interactions between nNOS and AMPA receptors have been reported [ 34 , 35 , 45 – 49 ]. Having established GluA1 as an S-nitrosylation target and considering the functional parallels between the NMDA receptor and Ca 2+ –permeable GluA1 AMPA receptors, we examined whether SAP97, closely related to PSD-95, could link AMPA receptors with nNOS.…”

Section: Resultsmentioning

confidence: 99%

Cysteine 893 is a target of regulatory thiol modifications of GluA1 AMPA receptors

Ossowski

Möykkynen

et al. 2017

PLoS ONE

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Recent studies indicate that glutamatergic signaling involves, and is regulated by, thiol modifying and redox-active compounds. In this study, we examined the role of a reactive cysteine residue, Cys-893, in the cytosolic C-terminal tail of GluA1 AMPA receptor as a potential regulatory target. Elimination of the thiol function by substitution of serine for Cys-893 led to increased steady-state expression level and strongly reduced interaction with SAP97, a major cytosolic interaction partner of GluA1 C-terminus. Moreover, we found that of the three cysteine residues in GluA1 C-terminal tail, Cys-893 is the predominant target for S-nitrosylation induced by exogenous nitric oxide donors in cultured cells and lysates. Co-precipitation experiments provided evidence for native association of SAP97 with neuronal nitric oxide synthase (nNOS) and for the potential coupling of Ca2+-permeable GluA1 receptors with nNOS via SAP97. Our results show that Cys-893 can serve as a molecular target for regulatory thiol modifications of GluA1 receptors, including the effects of nitric oxide.

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“…Next, cGKII phosphorylates GluA1 at the S845 site, initiating its incorporation into the membrane [70,71]. In addition, stimulation of the CP-AMPARs in the striatum neurons caused activation of neuronal NO synthase and cGMP production that also led to S845 GluA1 subunit phosphorylation and insertion of the receptor into the membrane [72].…”

Section: The Indirect Cgmp-dependent Pathwaymentioning

confidence: 99%

Modulation of AMPA Receptors by Nitric Oxide in Nerve Cells

Ivanova¹,

Balaban²,

Bal³

2020

IJMS

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Nitric oxide (NO) is a gaseous molecule with a large number of functions in living tissue. In the brain, NO participates in numerous intracellular mechanisms, including synaptic plasticity and cell homeostasis. NO elicits synaptic changes both through various multi-chain cascades and through direct nitrosylation of targeted proteins. Along with the N-methyl-d-aspartate (NMDA) glutamate receptors, one of the key components in synaptic functioning are α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors—the main target for long-term modifications of synaptic effectivity. AMPA receptors have been shown to participate in most of the functions important for neuronal activity, including memory formation. Interactions of NO and AMPA receptors were observed in important phenomena, such as glutamatergic excitotoxicity in retinal cells, synaptic plasticity, and neuropathologies. This review focuses on existing findings that concern pathways by which NO interacts with AMPA receptors, influences properties of different subunits of AMPA receptors, and regulates the receptors’ surface expression.

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Ca2+-permeable AMPA (α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid) Receptors and Dopamine D1 Receptors Regulate GluA1 Trafficking in Striatal Neurons

Abstract: Background: Trafficking of AMPA receptors (AMPAR) to medium spiny neuron (MSN) synapses regulates synapse strength. Results: The neurotransmitters dopamine and glutamate cooperate to induce MSN synaptic trafficking of the Ca

Cited by 19 publications

References 63 publications

Nucleus accumbens AMPA receptor trafficking upregulated by food restriction: an unintended target for drugs of abuse and forbidden foods

Nucleus accumbens AMPA receptor trafficking upregulated by food restriction: an unintended target for drugs of abuse and forbidden foods

Cysteine 893 is a target of regulatory thiol modifications of GluA1 AMPA receptors

Modulation of AMPA Receptors by Nitric Oxide in Nerve Cells

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