<i>Association</i> Basolateral amygdala stimulation evokes glutamate receptor‐dependent dopamine efflux in the nucleus accumbens of the anaesthetized rat

Floresco, Stan; Yang, Charles R.; Phillips, Anthony G.; Blaha, Charles D.

doi:10.1046/j.1460-9568.1998.00133.x

Cited by 150 publications

(121 citation statements)

References 63 publications

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“…As noted above, reciprocal innervation is evident also, and stimulating the afferent fibers from the amygdala and hippocampus increases accumbal DA release (Floresco et al, 1998;Floresco et al, 2001). Our finding of DA responses to cocaine cues in all three regions-amygdala, hippocampus, and striatum-supports the view of limbic and striatal structures as components of an integrated system, contributing to the incentive salience of motivationally relevant cues Phillips et al, 2003;Goto and Grace, 2008;Shohamy and Adcock, 2010).…”

Section: Discussionsupporting

confidence: 82%

Cocaine Cue-Induced Dopamine Release in Amygdala and Hippocampus: A High-Resolution PET [18F]Fallypride Study in Cocaine Dependent Participants

Fotros

Casey

Larcher

et al. 2013

Neuropsychopharmacol

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Drug-related cues are potent triggers for relapse in people with cocaine dependence. Dopamine (DA) release within a limbic network of striatum, amygdala and hippocampus has been implicated in animal studies, but in humans it has only been possible to measure effects in the striatum. The objective here was to measure drug cue-induced DA release in the amygdala and hippocampus using high-resolution PET with [ 18 F]fallypride. Twelve cocaine-dependent volunteers (mean age: 39.6 ± 8.0 years; years of cocaine use: 15.9 ± 7.4) underwent two [ 18 F]fallypride high-resolution research tomography-PET scans, one with exposure to neutral cues and one with cocaine cues. To our knowledge this study provides the first evidence of drug cue-induced DA release in the amygdala and hippocampus in humans. The preferential induction of DA release among high-craving responders suggests that these aspects of the limbic reward network might contribute to drug-seeking behavior.

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Section: Discussionsupporting

confidence: 82%

Cocaine Cue-Induced Dopamine Release in Amygdala and Hippocampus: A High-Resolution PET [18F]Fallypride Study in Cocaine Dependent Participants

Fotros

Casey

Larcher

et al. 2013

Neuropsychopharmacol

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“…Dopaminergic neurons in the VTA provide dopaminergic input to NAc and mPFC and receive glutamatergic input from several corticolimbic structures such as mPFC, amygdala, and hippocampus (48)(49)(50). Glutamatergic input to the VTA increases the activity of dopaminergic neurons and enhances dopamine release in NAc (51)(52)(53). Dopamine also affects glutamatergic transmission by increasing the firing probability in pyramidal neurons in mPFC (54).…”

Section: Discussionmentioning

confidence: 99%

WAVE1 in neurons expressing the D1 dopamine receptor regulates cellular and behavioral actions of cocaine

Ceglia

Lee

Cahill

et al. 2017

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

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Wiskott-Aldrich syndrome protein (WASP) family verprolin homologous protein 1 (WAVE1) regulates actin-related protein 2/3 (Arp2/3) complex-mediated actin polymerization. Our previous studies have found WAVE1 to be inhibited by Cdk5-mediated phosphorylation in brain and to play a role in the regulation of dendritic spine morphology. Here we report that mice in which WAVE1 was knocked out (KO) in neurons expressing the D1 dopamine receptor (D1-KO), but not mice where WAVE1 was knocked out in neurons expressing the D2 dopamine receptor (D2-KO), exhibited a significant decrease in place preference associated with cocaine. In contrast to wild-type (WT) and WAVE1 D2-KO mice, cocaine-induced sensitized locomotor behavior was not maintained in WAVE1 D1-KO mice. After chronic cocaine administration and following withdrawal, an acute cocaine challenge induced WAVE1 activation in striatum, which was assessed by dephosphorylation. The cocaine-induced WAVE1 dephosphorylation was attenuated by coadministration of either a D1 dopamine receptor or NMDA glutamate receptor antagonist. Upon an acute challenge of cocaine following chronic cocaine exposure and withdrawal, we also observed in WT, but not in WAVE1 D1-KO mice, a decrease in dendritic spine density and a decrease in the frequency of excitatory postsynaptic AMPA receptor currents in medium spiny projection neurons expressing the D1 dopamine receptor (D1-MSNs) in the nucleus accumbens. These results suggest that WAVE1 is involved selectively in D1-MSNs in cocaine-evoked neuronal activitymediated feedback regulation of glutamatergic synapses.W iskott-Aldrich syndrome protein (WASP) family verprolin homologous protein (WAVE) initiates de novo actin polymerization through its ability to activate the actin-related protein 2/3 (Arp2/3) complex (1). Three members of the family (WAVE1-3) exist, with WAVE1 being highly expressed in brain (2). WAVE1 was purified from bovine or rat brain as part of a heteropentameric protein complex together with PIR121 [also called cytoplasmic FMR1-interacting protein 2, (Cyfip2)], Nck-associated protein 1 (Nckap1), Abl-interactor 2 (Abi2), and HSPC300 (3, 4). Whereas WAVE1 plays a key role in Arp2/3 complex binding and actin polymerization, other protein components in the complex are important for its subcellular localization and interaction with upstream ligands or activators (5, 6).In our initial study in striatum, the WAVE1 complex was found to interact with p35, the regulatory subunit of cyclin-dependent kinase 5 (Cdk5) (4). Phosphorylation of WAVE1 at Ser310, Ser397, and Ser441 by Cdk5/p35, in the complex purified from rat brain, or with recombinant WAVE1, resulted in inhibition of actin polymerization in vitro (4). We also observed that the stoichiometry of WAVE1 phosphorylation by Cdk5 is high in brain, suggestive of the protein being largely inactive under basal conditions (4). However, studies using mouse striatal slices indicated that WAVE1 can be dephosphorylated at all three Cdk5 sites and thereby activated upon stimulation of D1 dopa...

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“…Furthermore, the glutamatergic terminals of BLA neurons projecting to the NAc synapse in close apposition to VTA-derived dopaminergic varicosities (Brog et al, 1993;Johnson et al, 1994;Phillips et al, 2003). These synapses are a possible site where the BLA glutamatergic projection can act presynaptically to increase dopamine efflux in the NAc (Floresco et al, 1998). These mutually facilitatory interactions between dopaminergic and glutamatergic afferents to the NAc may explain the similarity of the effects of NAc dopamine receptor antagonism and BLA inactivation on performance of the DS task.…”

Section: Inactivation Of the Blamentioning

confidence: 95%

Contributions of the amygdala and medial prefrontal cortex to incentive cue responding

et al. 2008

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Reward-seeking behavior is controlled by neuronal circuits that include the basolateral nucleus of amygdala (BLA), medial prefrontal cortex (mPFC), nucleus accumbens (NAc) and ventral tegmental area. Using a discriminative stimulus (DS) task in which an intermittently presented cue (DS) directs the animals to make an operant response for sucrose, we previously demonstrated that dopamine receptor antagonism in the NAc reduced reinforced cue responding, whereas general inactivation of the NAc increased behavioral responding in the absence of the cue. Because they send major glutamatergic projections to the NAc, the BLA and mPFC may also contribute to reward-seeking behaviors modulated by the NAc. In this study we compare the effects of BLA and mPFC inactivation on the performance of a DS task. BLA inactivation by combined GABA A and GABA B agonists impaired cue responding with minimal effects on operant behavior in the absence of cues. Dorsal mPFC (dmPFC) inactivation also inhibited cue-evoked reward-seeking. In contrast, ventral mPFC (vmPFC) inactivation disinhibited responding to unrewarded cues with less influence on reinforced cue responding. These findings demonstrate that the BLA and dmPFC facilitate cue-evoked rewardseeking, whereas, in the same task the vmPFC exerts inhibitory control over unrewarded behaviors.Keywords basolateral nucleus; infralimbic cortex; nucleus accumbens; prelimbic cortex; cingulate cortex; reward-seeking behavior Cue-evoked reward-seeking behaviors require recognition of learned cues that predict reward availability and selection of appropriate motor responses. Performance of reward-seeking behavior requires integrated functions of multiple brain areas including the basolateral nucleus of the amygdala (BLA), medial prefrontal cortex (mPFC), nucleus accumbens (NAc) and ventral tegmental area (VTA). The BLA and mPFC play crucial roles in reward-related © 2008 IBRO. Published by Elsevier Ltd. All rights reserved.Corresponding author: Akinori Ishikawa 1-1-1 Minamikogushi, Ube, Yamaguchi, 755-8505, Japan Phone: 81-836-22-2211 Fax: 81-836-22-2211.jp. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2010 July 9. Published in final edited form as:Neuroscience. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript behaviors and are major sources of glutamatergic afferents to the NAc (McGeorge and Faull, 1989;Brog et al., 1993;Zahm, 2000). The NAc, which receives excitatory inputs from the BLA and mPFC and projects via both direct and indir...

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Association Basolateral amygdala stimulation evokes glutamate receptor‐dependent dopamine efflux in the nucleus accumbens of the anaesthetized rat

Cited by 150 publications

References 63 publications

Cocaine Cue-Induced Dopamine Release in Amygdala and Hippocampus: A High-Resolution PET [18F]Fallypride Study in Cocaine Dependent Participants

Cocaine Cue-Induced Dopamine Release in Amygdala and Hippocampus: A High-Resolution PET [18F]Fallypride Study in Cocaine Dependent Participants

WAVE1 in neurons expressing the D1 dopamine receptor regulates cellular and behavioral actions of cocaine

Contributions of the amygdala and medial prefrontal cortex to incentive cue responding

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