Dopamine Receptor Stimulation Modulates AMPA Receptor Synaptic Insertion in Prefrontal Cortex Neurons

Sun, Xiu; Zhao, Yun; Wolf, Marina E.

doi:10.1523/jneurosci.4603-04.2005

Cited by 275 publications

(283 citation statements)

References 83 publications

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“…Broadly, some research on methamphetamine users has shown a decreased density of dopamine transporter in the striatum (e.g., Lundqvist 2005). As activation of DA receptors can modulate the expression of glutamate receptors, DA receptor activity can, in turn, alter synaptic plasticity (Sun et al 2005). LTP in the dentate gyrus was also found to be enhanced by amphetamine, in a dose-dependent manner (Gold et al 1984).…”

Section: Discussionmentioning

confidence: 99%

Memory and psychostimulants: modulation of Pavlovian fear conditioning by amphetamine in C57BL/6 mice

Wood

Anagnostaras

2008

Psychopharmacology

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Rationale and Objectives-With prescriptions of stimulants on the rise, it is important to examine the cognitive effects of low and moderate doses of stimulants, rather than only those typical of addicts.Methods-The present study examined the effects a range of doses (0.005 -8 mg/kg) of damphetamine sulfate on cued and contextual Pavlovian fear conditioning in mice.Results-In agreement with previous research, subjects administered a moderately high dose of amphetamine (8 mg/kg) pre-training, typical of what addicts might take, displayed impaired memory when tested, off-drug. Alternately, subjects injected with a very low dose of amphetamine (0.005, 0.025, or 0.05 mg/kg), pre-training, similar to the therapeutic doses for attention deficit hyperactivity disorder, displayed enhanced memory when tested, off-drug. A control study showed these effects were not due to state-dependent learning.Conclusions-Thus, dose is a critical determinant of the cognitive effects of psychostimulants.

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Section: Discussionmentioning

confidence: 99%

Memory and psychostimulants: modulation of Pavlovian fear conditioning by amphetamine in C57BL/6 mice

Wood

Anagnostaras

2008

Psychopharmacology

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“…Previous studies have shown that dopamine D1 receptor stimulation enhances GluR1 surface expression by activating cyclic adenosine monophosphate (cAMP) (15). We therefore postulated that GSK-3 inhibitors could also block dopamine/cAMP-induced insertion of GluR1 into the neuronal surface.…”

Section: Tat-klcpcdk Had Antidepressant-like and Antimanic-like Effecmentioning

confidence: 96%

A kinesin signaling complex mediates the ability of GSK-3β to affect mood-associated behaviors

Wei

Liu

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

113

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Lithium has been the gold standard in the treatment of bipolar disorder (BPD) for 60 y. Like lithium, glycogen synthase kinase 3 (GSK-3) inhibitors display both antimanic-like and antidepressant-like effects in some animal models. However, the molecular mechanisms of both lithium and GSK-3 inhibitors remain unclear. Here we show that the GSK-3 inhibitor AR-A014418 regulated α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA)-induced GluR1 and GluR2 internalization via phosphorylation of kinesin light chain 2 (KLC2), the key molecule of the kinesin cargo delivery system. Specifically, AMPA stimulation triggered serine phosphorylation of KLC2 and, subsequently, the dissociation of the GluR1/KLC2 protein complex. This suggests that GSK-3 phosphorylation of KLC2 led to the dissociation of AMPA-containing vesicles from the kinesin cargo system. The peptide TAT-KLCpCDK, a specific inhibitor for KLC2 phosphorylation by GSK-3β, reduced the formation of long-term depression. Furthermore, the TAT-KLCpCDK peptide showed antimanic-like effects similar to lithium's on amphetamine-induced hyperactivity, a frequently used animal model of mania. It also induced antidepressant-like effects in the tail suspension and forced swim tests, two commonly used animal models of depression. Taken together, the results demonstrated that KLC2 is a cellular target of GSK-3β capable of regulating synaptic plasticity, particularly AMPA receptor trafficking, as well as mood-associated behaviors in animal models. The kinesin cargo system may provide valuable novel targets for the development of new therapeutics for mood disorders.α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor | internalization | kinesin light chain 2

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“…The potential role of glutamatergic system in the pathophysiology of and treatment of mood disorders has been investigated in earnest only recently (Bonanno et al, 2005;Coyle and Duman, 2003;Du et al, 2004;Krystal et al, 2002;Sun et al, 2005). It is noteworthy that a growing body of data suggests that AMPA (-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptor trafficking (including receptor insertion, internalization, and delivery to synaptic sites) plays a critical role in regulating activity-dependent regulation of synaptic strength, as well as various forms of neural and behavioral plasticity (Bonanno et al, 2005;Carlezon and Nestler, 2002;Kendell et al, 2005;Malenka, 2003;Rumpel et al, 2005;Sun et al, 2005;Wolf et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

“…It is noteworthy that a growing body of data suggests that AMPA (-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptor trafficking (including receptor insertion, internalization, and delivery to synaptic sites) plays a critical role in regulating activity-dependent regulation of synaptic strength, as well as various forms of neural and behavioral plasticity (Bonanno et al, 2005;Carlezon and Nestler, 2002;Kendell et al, 2005;Malenka, 2003;Rumpel et al, 2005;Sun et al, 2005;Wolf et al, 2004). Three major classes of ionotropic glutamate receptors are expressed throughout the mammalian central nervous system (CNS), including AMPA, kainate, and N-methyl-Daspartate (NMDA) receptors.…”

Section: Introductionmentioning

confidence: 99%

The Anticonvulsants Lamotrigine, Riluzole, and Valproate Differentially Regulate AMPA Receptor Membrane Localization: Relationship to Clinical Effects in Mood Disorders

Suzuki

Wei

et al. 2006

Neuropsychopharmacol

190

152

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A growing body of data suggests that the glutamatergic system may be involved in the pathophysiology and treatment of severe mood disorders. Chronic treatment with the antimanic agents, lithium and valproate, resulted in reduced synaptic expression of the AMPA(-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptor subunit GluR1 in the hippocampus, while treatment with an antidepressant (imipramine) enhanced the synaptic expression of GluR1. The anticonvulsants, lamotrigine (6-(2,3-dichlorophenyl)-1,2,4-triazine-3,5-diamine) and riluzole (2-amino-6-trifluoromethoxybenzothiazole), have been demonstrated to have efficacy in the depressive phase of bipolar disorder. We therefore sought to determine the role of these anticonvulsants, compared to that of the predominantly antimanic anticonvulsant valproate, on AMPA receptor localization. We found that the agents with a predominantly antidepressant profile, namely lamotrigine and riluzole, significantly enhanced the surface expression of GluR1 and GluR2 in a time-and dose-dependent manner in cultured hippocampal neurons. By contrast, the predominantly antimanic agent, valproate, significantly reduced surface expression of GluR1 and GluR2. Concomitant with the GluR1 and GluR2 changes, the peak value of depolarized membrane potential evoked by AMPA was significantly higher in lamotrigine-and riluzole-treated neurons, supporting the surface receptor changes. Phosphorylation of GluR1 at the PKA (cAMP-dependent protein kinase) site (S845) was enhanced in both lamotrigine-and riluzoletreated hippocampal neurons, but reduced in valproate-treated neurons. In addition, lamotrigine and riluzole, as well as the traditional antidepressant imipramine, also increased GluR1 phosphorylation at GluR1 (S845) in the hippocampus after chronic in vivo treatment. Our findings suggest that regulation of GluR1/2 surface levels and function may be responsible for the different clinical profile of anticonvulsants (antimanic or antidepressant), and may suggest avenues for the development of novel therapeutics for these illnesses.

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Dopamine Receptor Stimulation Modulates AMPA Receptor Synaptic Insertion in Prefrontal Cortex Neurons

Cited by 275 publications

References 83 publications

Memory and psychostimulants: modulation of Pavlovian fear conditioning by amphetamine in C57BL/6 mice

Memory and psychostimulants: modulation of Pavlovian fear conditioning by amphetamine in C57BL/6 mice

A kinesin signaling complex mediates the ability of GSK-3β to affect mood-associated behaviors

The Anticonvulsants Lamotrigine, Riluzole, and Valproate Differentially Regulate AMPA Receptor Membrane Localization: Relationship to Clinical Effects in Mood Disorders

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