Schlüter, Oliver M.

[["dc.bibliographiccitation.firstpage","1644"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","1651"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Lee, Brian R."],["dc.contributor.author","Ma, Yao-Ying"],["dc.contributor.author","Huang, Yanhua H."],["dc.contributor.author","Wang, Xiusong"],["dc.contributor.author","Otaka, Mami"],["dc.contributor.author","Ishikawa, Masago"],["dc.contributor.author","Neumann, Peter A."],["dc.contributor.author","Graziane, Nicholas M."],["dc.contributor.author","Brown, Travis E."],["dc.contributor.author","Suska, Anna"],["dc.contributor.author","Guo, Changyong"],["dc.contributor.author","Lobo, Mary Kay"],["dc.contributor.author","Sesack, Susan R."],["dc.contributor.author","Wolf, Marina E."],["dc.contributor.author","Nestler, Eric J."],["dc.contributor.author","Shaham, Yavin"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.date.accessioned","2021-04-27T14:47:29Z"],["dc.date.available","2021-04-27T14:47:29Z"],["dc.date.issued","2013-11"],["dc.description.abstract","In rat models of drug relapse and craving, cue-induced cocaine seeking progressively increases after withdrawal from the drug. This 'incubation of cocaine craving' is partially mediated by time-dependent adaptations at glutamatergic synapses in nucleus accumbens (NAc). However, the circuit-level adaptations mediating this plasticity remain elusive. We studied silent synapses, often regarded as immature synapses that express stable NMDA receptors with AMPA receptors being either absent or labile, in the projection from the basolateral amygdala to the NAc in incubation of cocaine craving. Silent synapses were detected in this projection during early withdrawal from cocaine. As the withdrawal period progressed, these silent synapses became unsilenced, a process that involved synaptic insertion of calcium-permeable AMPA receptors (CP-AMPARs). In vivo optogenetic stimulation-induced downregulation of CP-AMPARs at amygdala-to-NAc synapses, which re-silenced some of the previously silent synapses after prolonged withdrawal, decreased incubation of cocaine craving. Our findings indicate that silent synapse-based reorganization of the amygdala-to-NAc projection is critical for persistent cocaine craving and relapse after withdrawal."],["dc.identifier.doi","10.1038/nn.3533"],["dc.identifier.pmid","24077564"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84488"],["dc.language.iso","en"],["dc.relation.eissn","1546-1726"],["dc.relation.issn","1097-6256"],["dc.title","Maturation of silent synapses in amygdala-accumbens projection contributes to incubation of cocaine craving"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5820"],["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","5831"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Ishikawa, Masago"],["dc.contributor.author","Mu, Ping"],["dc.contributor.author","Moyer, Jason T."],["dc.contributor.author","Wolf, John A."],["dc.contributor.author","Quock, Raymond M."],["dc.contributor.author","Davies, Neal M."],["dc.contributor.author","Hu, Xiu-Ti"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.date.accessioned","2021-04-27T14:47:02Z"],["dc.date.available","2021-04-27T14:47:02Z"],["dc.date.issued","2009-05-06"],["dc.description.abstract","Stable brain function relies on homeostatic maintenance of the functional output of individual neurons. In general, neurons function by converting synaptic input to output as action potential firing. To determine homeostatic mechanisms that balance this input-output/synapse-membrane interaction, we focused on nucleus accumbens (NAc) neurons and demonstrated a novel form of synapse-to-membrane homeostatic regulation, homeostatic synapse-driven membrane plasticity (hSMP). Through hSMP, NAc neurons adjusted their membrane excitability to functionally compensate for basal shifts in excitatory synaptic input. Furthermore, hSMP was triggered by synaptic NMDA receptors (NMDARs) and expressed by the modification of SK-type Ca(2+)-activated potassium channels. Moreover, hSMP in NAc neurons was abolished in rats during a short- (2 d) or long- (21 d) term withdrawal from repeated intraperitoneal injections of cocaine (15 mg/kg/d, 5 d). These results suggest that hSMP is a novel form of synapse-to-membrane homeostatic plasticity and dysregulation of hSMP may contribute to cocaine-induced cellular alterations in the NAc."],["dc.identifier.doi","10.1523/JNEUROSCI.5703-08.2009"],["dc.identifier.pmid","19420249"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84482"],["dc.language.iso","en"],["dc.relation.eissn","1529-2401"],["dc.relation.issn","0270-6474"],["dc.title","Homeostatic synapse-driven membrane plasticity in nucleus accumbens neurons"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","18453"],["dc.bibliographiccitation.issue","50"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","18463"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Huang, Yanhua H."],["dc.contributor.author","Ishikawa, Masago"],["dc.contributor.author","Lee, Brian R"],["dc.contributor.author","Nakanishi, Nobuki"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.date.accessioned","2021-04-27T14:46:33Z"],["dc.date.available","2021-04-27T14:46:33Z"],["dc.date.issued","2011-12-14"],["dc.description.abstract","The nucleus accumbens shell (NAc) is a key brain region mediating emotional and motivational learning. In rodent models, dynamic alterations have been observed in synaptic NMDA receptors (NMDARs) within the NAc following incentive stimuli, and some of these alterations are critical for acquiring new emotional/motivational states. NMDARs are prominent molecular devices for controlling neural plasticity and memory formation. Although synaptic NMDARs are predominately located postsynaptically, recent evidence suggests that they may also exist at presynaptic terminals and reshape excitatory synaptic transmission by regulating presynaptic glutamate release. However, it remains unknown whether presynaptic NMDARs exist in the NAc and contribute to emotional and motivational learning. In an attempt to identify presynaptically located NMDARs in the NAc, the present study uses slice electrophysiology combined with pharmacological and genetic tools to examine the physiological role of the putative presynaptic NMDARs in rats. Our results show that application of glycine, the glycine-site agonist of NMDARs, potentiated presynaptic release of glutamate at excitatory synapses on NAc neurons, whereas application of 5,7-dichlorokynurenic acid or 7-chlorokynurenic acid, the glycine-site antagonists of NMDARs, produced the opposite effect. However, these seemingly presynaptic NMDAR-mediated effects could not be prevented by application of d-APV, the glutamate-site NMDAR antagonist, and were still present in the mice in which NMDAR NR1 or NR3 subunits were genetically deleted. Thus, rather than suggesting the existence of presynaptic NMDARs, our results support the idea that an unidentified type of glycine-activated substrate may account for the presynaptic effects appearing to be mediated by NMDARs."],["dc.identifier.doi","10.1523/JNEUROSCI.3824-11.2011"],["dc.identifier.pmid","22171047"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84476"],["dc.language.iso","en"],["dc.relation.eissn","1529-2401"],["dc.relation.issn","0270-6474"],["dc.title","Searching for presynaptic NMDA receptors in the nucleus accumbens"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6753"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","6758"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Otaka, Mami"],["dc.contributor.author","Ishikawa, Masago"],["dc.contributor.author","Lee, Brian R."],["dc.contributor.author","Liu, Lei"],["dc.contributor.author","Neumann, Peter A."],["dc.contributor.author","Cui, Ranji"],["dc.contributor.author","Huang, Yanhua H."],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.date.accessioned","2021-04-27T14:46:42Z"],["dc.date.available","2021-04-27T14:46:42Z"],["dc.date.issued","2013-04-17"],["dc.description.abstract","Medium spiny neurons (MSNs) within the nucleus accumbens shell (NAc) function to gate and prioritize emotional/motivational arousals for behavioral output. The neuronal output of NAc MSNs is mainly determined by the integration of membrane excitability and excitatory/inhibitory synaptic inputs. Whereas cocaine-induced alterations at excitatory synapses and membrane excitability have been extensively examined, the overall functional output of NAc MSNs following cocaine exposure is still poorly defined because little is known about whether inhibitory synaptic input to these neurons is affected by cocaine. Here, our results demonstrate multidimensional alterations at inhibitory synapses in NAc neurons following cocaine self-administration in rats. Specifically, the amplitude of miniature IPSCs (mIPSCs) was decreased after 21 d withdrawal from 5 d cocaine self-administration. Upon re-exposure to cocaine after 21 d withdrawal, whereas the amplitude of mIPSCs remained downregulated, the frequency became significantly higher. Furthermore, the reversal potential of IPSCs, which was not significantly altered during withdrawal, became more hyperpolarized upon cocaine re-exposure. Moreover, the relative weight of excitatory and inhibitory inputs to NAc MSNs was significantly decreased after 1 d cocaine withdrawal, increased after 21 d withdrawal, and returned to the basal level upon cocaine re-exposure after 21 d withdrawal. These results, together with previous results showing cocaine-induced adaptations at excitatory synapses and intrinsic membrane excitability of NAc MSNs, may provide a relatively thorough picture of the functional state of NAc MSNs following cocaine exposure."],["dc.identifier.doi","10.1523/JNEUROSCI.4577-12.2013"],["dc.identifier.pmid","23595733"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84478"],["dc.language.iso","en"],["dc.relation.eissn","1529-2401"],["dc.relation.issn","0270-6474"],["dc.title","Exposure to cocaine regulates inhibitory synaptic transmission in the nucleus accumbens"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8163"],["dc.bibliographiccitation.issue","22"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","8174"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Brown, Travis E."],["dc.contributor.author","Lee, Brian R."],["dc.contributor.author","Mu, Ping"],["dc.contributor.author","Ferguson, Deveroux"],["dc.contributor.author","Dietz, David"],["dc.contributor.author","Ohnishi, Yoshinori N."],["dc.contributor.author","Lin, Ying"],["dc.contributor.author","Suska, Anna"],["dc.contributor.author","Ishikawa, Masago"],["dc.contributor.author","Huang, Yanhua H."],["dc.contributor.author","Shen, Haowei"],["dc.contributor.author","Kalivas, Peter W."],["dc.contributor.author","Sorg, Barbara A."],["dc.contributor.author","Zukin, R. Suzanne"],["dc.contributor.author","Nestler, Eric J."],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Schlueter, Oliver M."],["dc.date.accessioned","2018-11-07T08:55:35Z"],["dc.date.available","2018-11-07T08:55:35Z"],["dc.date.issued","2011"],["dc.description.abstract","Locomotor sensitization is a common and robust behavioral alteration in rodents whereby following exposure to abused drugs such as cocaine, the animal becomes significantly more hyperactive in response to an acute drug challenge. Here, we further analyzed the role of cocaine-induced silent synapses in the nucleus accumbens (NAc) shell and their contribution to the development of locomotor sensitization. Using a combination of viral vector-mediated genetic manipulations, biochemistry, and electrophysiology in a locomotor sensitization paradigm with repeated, daily, noncontingent cocaine (15 mg/kg) injections, we show that dominant-negative cAMP-element binding protein (CREB) prevents cocaine-induced generation of silent synapses of young (30 d old) rats, whereas constitutively active CREB is sufficient to increase the number of NR2B-containing NMDA receptors (NMDARs) at synapses and to generate silent synapses. We further show that occupancy of CREB at the NR2B promoter increases and is causally related to the increase in synaptic NR2B levels. Blockade of NR2B-containing NMDARs by administration of the NR2B-selective antagonist Ro256981 directly into the NAc, under conditions that inhibit cocaine-induced silent synapses, prevents the development of cocaine-elicited locomotor sensitization. Our data are consistent with a cellular cascade whereby cocaine-induced activation of CREB promotes CREB-dependent transcription of NR2B and synaptic incorporation of NR2B-containing NMDARs, which generates new silent synapses within the NAc. We propose that cocaine-induced activation of CREB and generation of new silent synapses may serve as key cellular events mediating cocaine-induced locomotor sensitization. These findings provide a novel cellular mechanism that may contribute to cocaine-induced behavioral alterations."],["dc.identifier.doi","10.1523/JNEUROSCI.0016-11.2011"],["dc.identifier.isi","000291208100023"],["dc.identifier.pmid","21632938"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22942"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","A Silent Synapse-Based Mechanism for Cocaine-Induced Locomotor Sensitization"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6759"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","6765"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Ishikawa, Masago"],["dc.contributor.author","Otaka, Mami"],["dc.contributor.author","Huang, Yanhua H."],["dc.contributor.author","Neumann, Peter A."],["dc.contributor.author","Winters, Bradley D."],["dc.contributor.author","Grace, Anthony A."],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.date.accessioned","2021-04-27T14:46:47Z"],["dc.date.available","2021-04-27T14:46:47Z"],["dc.date.issued","2013-04-17"],["dc.description.abstract","As a classic neuromodulator, dopamine has long been thought to modulate, rather than trigger, synaptic plasticity. In contrast, our present results demonstrate that within the parallel projections of dopaminergic and GABAergic terminals from the ventral tegmental area to the nucleus accumbens core (NAcCo), action-potential-activated release of dopamine heterosynaptically triggers LTD at GABAergic synapses, which is likely mediated by activating presynaptically located dopamine D1 class receptors and expressed by inhibiting presynaptic release of GABA. Moreover, this dopamine-mediated heterosynaptic LTD is abolished after withdrawal from cocaine exposure. These results suggest that action-potential-dependent dopamine release triggers very different cellular consequences from those induced by volume release or pharmacological manipulation. Activation of the ventral tegmental area to NAcCo projections is essential for emotional and motivational responses. This dopamine-mediated LTD allows a flexible output of NAcCo neurons, whereas disruption of this LTD may contribute to the rigid emotional and motivational state observed in addicts during cocaine withdrawal."],["dc.identifier.doi","10.1523/JNEUROSCI.4694-12.2013"],["dc.identifier.pmid","23595734"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84479"],["dc.language.iso","en"],["dc.relation.eissn","1529-2401"],["dc.relation.issn","0270-6474"],["dc.title","Dopamine triggers heterosynaptic plasticity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4316"],["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","4328"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Wang, Junshi"],["dc.contributor.author","Ishikawa, Masago"],["dc.contributor.author","Yang, Yue"],["dc.contributor.author","Otaka, Mami"],["dc.contributor.author","Kim, James Y."],["dc.contributor.author","Gardner, George R."],["dc.contributor.author","Stefanik, Michael T."],["dc.contributor.author","Milovanovic, Mike"],["dc.contributor.author","Huang, Yanhua H."],["dc.contributor.author","Hell, Johannes W."],["dc.contributor.author","Wolf, Marina E."],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.date.accessioned","2021-04-27T14:46:38Z"],["dc.date.available","2021-04-27T14:46:38Z"],["dc.date.issued","2018"],["dc.description.abstract","In human drug users, cue-induced drug craving progressively intensifies after drug abstinence, promoting drug relapse. This time-dependent progression of drug craving is recapitulated in rodent models, in which rats exhibit progressive intensification of cue-induced drug seeking after withdrawal from drug self-administration, a phenomenon termed incubation of drug craving. Although recent results suggest that functional alterations of the nucleus accumbens (NAc) contribute to incubation of drug craving, it remains poorly understood how NAc function evolves after drug withdrawal to progressively intensify drug seeking. The functional output of NAc relies on how the membrane excitability of its principal medium spiny neurons (MSNs) translates excitatory synaptic inputs into action potential firing. Here, we report a synapse-membrane homeostatic crosstalk (SMHC) in male rats, through which an increase or decrease in the excitatory synaptic strength induces a homeostatic decrease or increase in the intrinsic membrane excitability of NAc MSNs, and vice versa. After short-term withdrawal from cocaine self-administration, despite no actual change in the AMPA receptor-mediated excitatory synaptic strength, GluN2B NMDA receptors, the SMHC sensors of synaptic strength, are upregulated. This may create false SMHC signals, leading to a decrease in the membrane excitability of NAc MSNs. The decreased membrane excitability subsequently induces another round of SMHC, leading to synaptic accumulation of calcium-permeable AMPA receptors and upregulation of excitatory synaptic strength after long-term withdrawal from cocaine. Disrupting SMHC-based dysregulation cascades after cocaine exposure prevents incubation of cocaine craving. Thus, cocaine triggers cascades of SMHC-based dysregulation in NAc MSNs, promoting incubated cocaine seeking after drug withdrawal.SIGNIFICANCE STATEMENT Here, we report a bidirectional homeostatic plasticity between the excitatory synaptic input and membrane excitability of nucleus accumbens (NAc) medium spiny neurons (MSNs), through which an increase or decrease in the excitatory synaptic strength induces a homeostatic decrease or increase in the membrane excitability, and vice versa. Cocaine self-administration creates a false homeostatic signal that engages this synapse-membrane homeostatic crosstalk mechanism, and produces cascades of alterations in excitatory synapses and membrane properties of NAc MSNs after withdrawal from cocaine. Experimentally preventing this homeostatic dysregulation cascade prevents the progressive intensification of cocaine seeking after drug withdrawal. These results provide a novel mechanism through which drug-induced homeostatic dysregulation cascades progressively alter the functional output of NAc MSNs and promote drug relapse."],["dc.identifier.doi","10.1523/JNEUROSCI.3291-17.2018"],["dc.identifier.pmid","29626166"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84477"],["dc.language.iso","en"],["dc.relation.eissn","1529-2401"],["dc.relation.issn","0270-6474"],["dc.title","Cascades of Homeostatic Dysregulation Promote Incubation of Cocaine Craving"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3689"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","The Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","3699"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Mu, Ping"],["dc.contributor.author","Moyer, Jason T."],["dc.contributor.author","Ishikawa, Masago"],["dc.contributor.author","Zhang, Yonghong"],["dc.contributor.author","Panksepp, Jaak"],["dc.contributor.author","Sorg, Barbara A."],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.date.accessioned","2021-04-27T14:46:56Z"],["dc.date.available","2021-04-27T14:46:56Z"],["dc.date.issued","2010-03-10"],["dc.description.abstract","Drug-induced malfunction of nucleus accumbens (NAc) neurons underlies a key pathophysiology of drug addiction. Drug-induced changes in intrinsic membrane excitability of NAc neurons are thought to be critical for producing behavioral alterations. Previous studies demonstrate that, after short-term (2 d) or long-term (21 d) withdrawal from noncontingent cocaine injection, the intrinsic membrane excitability of NAc shell (NAcSh) neurons is decreased, and decreased membrane excitability of NAcSh neurons increases the acute locomotor response to cocaine. However, animals exhibit distinct cellular and behavioral alterations at different stages of cocaine exposure, suggesting that the decreased membrane excitability of NAc neurons may not be a persistent change. Here, we demonstrate that the membrane excitability of NAcSh neurons is differentially regulated depending on whether cocaine is administered contingently or noncontingently. Specifically, the membrane excitability of NAcSh medium spiny neurons (MSNs) was decreased at 2 d after withdrawal from either 5 d intraperitoneal injections (15 mg/kg) or cocaine self-administration (SA). At 21 d of withdrawal, the membrane excitability of NAcSh MSNs, which remained low in intraperitoneally pretreated rats, returned to a normal level in SA-pretreated rats. Furthermore, after a reexposure to cocaine after long-term withdrawal, the membrane excitability of NAcSh MSNs instantly returned to a normal level in intraperitoneally pretreated rats. Conversely, in SA-pretreated rats, the reexposure elevated the membrane excitability of NAcSh MSMs beyond the normal level. These results suggest that the dynamic alterations in membrane excitability of NAcSh MSNs, together with the dynamic changes in synaptic input, contribute differentially to the behavioral consequences of contingent and noncontingent cocaine administration."],["dc.identifier.doi","10.1523/JNEUROSCI.4063-09.2010"],["dc.identifier.pmid","20220002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84481"],["dc.language.iso","en"],["dc.relation.eissn","1529-2401"],["dc.relation.issn","0270-6474"],["dc.title","Exposure to cocaine dynamically regulates the intrinsic membrane excitability of nucleus accumbens neurons"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2399"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","2410"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Neumann, Peter A."],["dc.contributor.author","Wang, Yicun"],["dc.contributor.author","Yan, Yijin"],["dc.contributor.author","Wang, Yao"],["dc.contributor.author","Ishikawa, Masago"],["dc.contributor.author","Cui, Ranji"],["dc.contributor.author","Huang, Yanhua H."],["dc.contributor.author","Sesack, Susan R."],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.date.accessioned","2021-04-27T14:47:44Z"],["dc.date.available","2021-04-27T14:47:44Z"],["dc.date.issued","2016"],["dc.description.abstract","Exposure to cocaine induces addiction-associated behaviors partially through remodeling neurocircuits in the nucleus accumbens (NAc). The paraventricular nucleus of thalamus (PVT), which projects to the NAc monosynaptically, is activated by cocaine exposure and has been implicated in several cocaine-induced emotional and motivational states. Here we show that disrupting synaptic transmission of select PVT neurons with tetanus toxin activated via retrograde trans-synaptic transport of cre from NAc efferents decreased cocaine self-administration in rats. This projection underwent complex adaptations after self-administration of cocaine (0.75 mg/kg/infusion; 2 h/d × 5 d, 1d overnight training). Specifically, 1d after cocaine self-administration, we observed increased levels of AMPA receptor (AMPAR)-silent glutamatergic synapses in this projection, accompanied by a decreased ratio of AMPAR-to-NMDA receptor (NMDAR)-mediated EPSCs. Furthermore, the decay kinetics of NMDAR EPSCs was significantly prolonged, suggesting insertion of new GluN2B-containing NMDARs to PVT-to-NAc synapses. After 45-d withdrawal, silent synapses within this projection returned to the basal levels, accompanied by a return of the AMPAR/NMDAR ratio and NMDAR decay kinetics to the basal levels. In amygdala and infralimbic prefrontal cortical projections to the NAc, a portion of cocaine-generated silent synapses becomes unsilenced by recruiting calcium-permeable AMPARs (CP-AMPARs) after drug withdrawal. However, the sensitivity of PVT-to-NAc synapses to CP-AMPAR-selective antagonists was not changed after withdrawal, suggesting that CP-AMPAR trafficking is not involved in the evolution of cocaine-generated silent synapses within this projection. Meanwhile, the release probability of PVT-to-NAc synapses was increased after short- and long-term cocaine withdrawal. These results reveal complex and profound alterations at PVT-to-NAc synapses after cocaine exposure and withdrawal."],["dc.identifier.doi","10.1038/npp.2016.52"],["dc.identifier.pmid","27074816"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84491"],["dc.language.iso","en"],["dc.relation.eissn","1740-634X"],["dc.relation.issn","0893-133X"],["dc.title","Cocaine-Induced Synaptic Alterations in Thalamus to Nucleus Accumbens Projection"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","386"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Biological Psychiatry"],["dc.bibliographiccitation.lastpage","397"],["dc.bibliographiccitation.volume","89"],["dc.contributor.author","Wang, Junshi"],["dc.contributor.author","Li, King-Lun"],["dc.contributor.author","Shukla, Avani"],["dc.contributor.author","Beroun, Ania"],["dc.contributor.author","Ishikawa, Masago"],["dc.contributor.author","Huang, Xiaojie"],["dc.contributor.author","Wang, Yao"],["dc.contributor.author","Wang, Yao Q."],["dc.contributor.author","Yang, Yue"],["dc.contributor.author","Bastola, Noah D."],["dc.contributor.author","Huang, Hugh H."],["dc.contributor.author","Kramer, Lily E."],["dc.contributor.author","Chao, Terry"],["dc.contributor.author","Huang, Yanhua H."],["dc.contributor.author","Sesack, Susan R."],["dc.contributor.author","Nestler, Eric J."],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.date.accessioned","2021-04-14T08:29:04Z"],["dc.date.available","2021-04-14T08:29:04Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1016/j.biopsych.2020.08.012"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82785"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","0006-3223"],["dc.title","Cocaine Triggers Astrocyte-Mediated Synaptogenesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]