Schlüter, Oliver M.

[["dc.bibliographiccitation.firstpage","228"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Biological Psychiatry"],["dc.bibliographiccitation.lastpage","235"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Mu, Ping"],["dc.contributor.author","Neumann, Peter A."],["dc.contributor.author","Panksepp, Jaak"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.date.accessioned","2021-04-27T14:48:59Z"],["dc.date.available","2021-04-27T14:48:59Z"],["dc.date.issued","2011-02-01"],["dc.description.abstract","Dysregulation of excitatory synaptic input to nucleus accumbens (NAc) medium spiny neurons (MSNs) underlies a key pathophysiology of drug addiction and addiction-associated emotional and motivational alterations. Dynorphin peptides, which exhibit higher affinity to κ type opioid receptors, are upregulated within the NAc upon exposure to cocaine administration, and the increased dynorphin-signaling in the NAc has been critically implicated in negative mood observed in cocaine- or stress-exposed animals. Despite such apparent behavioral significance of the NAc dynorphins, the understanding of how dynorphins regulate excitatory synaptic transmission in the NAc remains incomplete."],["dc.identifier.doi","10.1016/j.biopsych.2010.09.014"],["dc.identifier.pmid","21030009"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84507"],["dc.language.iso","en"],["dc.relation.eissn","1873-2402"],["dc.relation.issn","0006-3223"],["dc.title","Exposure to cocaine alters dynorphin-mediated regulation of excitatory synaptic transmission in nucleus accumbens neurons"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","15504"],["dc.bibliographiccitation.issue","39"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","15517"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Krueger, Juliane M."],["dc.contributor.author","Favaro, Plinio D."],["dc.contributor.author","Liu, Mingna"],["dc.contributor.author","Kitlinska, Agata"],["dc.contributor.author","Huang, Xiaojie"],["dc.contributor.author","Raabe, Monika"],["dc.contributor.author","Akad, Derya S."],["dc.contributor.author","Liu, Yanling"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Xu, Weifeng"],["dc.contributor.author","Schlueter, Oliver M."],["dc.date.accessioned","2018-11-07T09:19:47Z"],["dc.date.available","2018-11-07T09:19:47Z"],["dc.date.issued","2013"],["dc.description.abstract","In the postsynaptic density of glutamatergic synapses, the discs large (DLG)-membrane-associated guanylate kinase (MAGUK) family of scaffolding proteins coordinates a multiplicity of signaling pathways to maintain and regulate synaptic transmission. Postsynaptic density-93 (PSD-93) is the most variable paralog in this family; it exists in six different N-terminal isoforms. Probably because of the structural and functional variability of these isoforms, the synaptic role of PSD-93 remains controversial. To accurately characterize the synaptic role of PSD-93, we quantified the expression of all six isoforms in the mouse hippocampus and examined them individually in hippocampal synapses. Using molecular manipulations, including overexpression, gene knockdown, PSD-93 knock-out mice combined with biochemical assays, and slice electrophysiology both in rat and mice, we demonstrate that PSD-93 is required at different developmental synaptic states to maintain the strength of excitatory synaptic transmission. This strength is differentially regulated by the six isoforms of PSD-93, including regulations of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor-active and inactive synapses, and activity-dependent modulations. Collectively, these results demonstrate that alternative combinations of N-terminal PSD-93 isoforms and DLG-MAGUK paralogs can fine-tune signaling scaffolds to adjust synaptic needs to regulate synaptic transmission."],["dc.identifier.doi","10.1523/JNEUROSCI.0019-12.2013"],["dc.identifier.isi","000324912500021"],["dc.identifier.pmid","24068818"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28724"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","Differential Roles of Postsynaptic Density-93 Isoforms in Regulating Synaptic Transmission"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","451"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","The Neuroscientist"],["dc.bibliographiccitation.lastpage","459"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Huang, Yanhua H."],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.date.accessioned","2021-04-27T14:48:29Z"],["dc.date.available","2021-04-27T14:48:29Z"],["dc.date.issued","2015-10"],["dc.description.abstract","A transient but prominent increase in the level of \"silent synapses\"--a signature of immature glutamatergic synapses that contain only NMDA receptors without stably expressed AMPA receptors--has been identified in the nucleus accumbens (NAc) following exposure to cocaine. As the NAc is a critical forebrain region implicated in forming addiction-associated behaviors, the initial discoveries have raised speculations about whether and how these drug-induced synapses mature and potentially contribute to addiction-related behaviors. Here, we summarize recent progress in recognizing the pathway-specific regulations of silent synapse maturation, and its diverse impacts on behavior. We provide an update of the guiding hypothesis--the \"neural rejuvenation hypothesis\"--with recently emerged evidence of silent synapses in cocaine craving and relapse."],["dc.identifier.doi","10.1177/1073858415579405"],["dc.identifier.pmid","25829364"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84501"],["dc.language.iso","en"],["dc.relation.eissn","1089-4098"],["dc.relation.issn","1073-8584"],["dc.title","Silent Synapses Speak Up: Updates of the Neural Rejuvenation Hypothesis of Drug Addiction"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","13398"],["dc.bibliographiccitation.issue","33"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","13409"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Bonnet, Stephanie A. D."],["dc.contributor.author","Akad, Derya S."],["dc.contributor.author","Samaddar, Tanmoy"],["dc.contributor.author","Liu, Yanling"],["dc.contributor.author","Huang, Xiaojie"],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Schlueter, Oliver M."],["dc.date.accessioned","2018-11-07T09:21:16Z"],["dc.date.available","2018-11-07T09:21:16Z"],["dc.date.issued","2013"],["dc.description.abstract","Activity-dependent regulation of AMPA receptor (AMPAR)-mediated synaptic transmission is the basis for establishing differences in synaptic weights among individual synapses during developmental and experience-dependent synaptic plasticity. Synaptic signaling scaffolds of the Discs large (DLG)-membrane-associated guanylate kinase(MAGUK) protein family regulate these processes by tethering signaling proteins to receptor complexes. Using a molecular replacement strategy with RNAi-mediated knockdown in rat and mouse hippocampal organotypic slice cultures, a postsynaptic density-95 (PSD-95) knock-out mouse line and electrophysiological analysis, our current study identified a functional interplay between two paralogs, PSD-95 and synapse-associated protein 102 (SAP102) to regulate synaptic AMPARs. During synaptic development, the SAP102 protein levels normally plateau but double if PSD-95 expression is prevented during synaptogenesis. For an autonomous function of PSD-95 in regulating synaptic AMPARs, in addition to the previously demonstrated N-terminal multimerization and the first two PDZ (PSD-95, Dlg1, zona occludens-1) domains, the PDZ3 and guanylate kinase domains were required. The Src homology 3 domain was dispensable for the PSD-95-autonomous regulation of basal synaptic transmission. However, it mediated the functional interaction with SAP102 of PSD-95 mutants to enhance AMPARs. These results depict a protein domain-based multifunctional aspect of PSD-95 in regulating excitatory synaptic transmission and unveil a novel form of domain-based interplay between signaling scaffolds of the DLG-MAGUK family."],["dc.identifier.doi","10.1523/JNEUROSCI.6255-11.2013"],["dc.identifier.isi","000323155700014"],["dc.identifier.pmid","23946397"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29074"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","Synaptic State-Dependent Functional Interplay between Postsynaptic Density-95 and Synapse-Associated Protein 102"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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","2240"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","2248"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Chen, Bo"],["dc.contributor.author","Ma, Yao-Ying"],["dc.contributor.author","Wang, Yao"],["dc.contributor.author","Wang, Xiusong"],["dc.contributor.author","Schlüter, Oliver M."],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Huang, Yanhua H."],["dc.date.accessioned","2021-04-27T14:48:49Z"],["dc.date.available","2021-04-27T14:48:49Z"],["dc.date.issued","2013-10"],["dc.description.abstract","Exposure to drugs of abuse lead to both rewarding effects and the subsequent development of negative affects. The progressive dysregulation of both processes is thought to critically contribute to the addictive state. Whereas cocaine-induced maladaptations in reward circuitry have been extensively examined, the cellular substrates underlying negative affect remain poorly understood. This study focuses on the central nucleus of the amygdala (CeA), a brain region that has been implicated in negative affective states upon withdrawal from chronic cocaine use. We observed that the two major types of CeA neurons, low-threshold bursting (LTB) neurons and regular spiking (RS) neurons, exhibited different sensitivity to corticotrophin-releasing factor (CRF), a stress hormone that has been implicated in negative affect during drug withdrawal. Furthermore, LTB and RS neurons developed opposite membrane adaptations following short-term (5 day) cocaine self-administration; the membrane excitability was increased in LTB neurons but decreased in RS neurons. These short-term exposure-induced effects were transient as they were present on withdrawal day 1 but disappeared on withdrawal day 21. However, extended exposure (21 day) led to sustained increase in the membrane excitability of LTB neurons such that it lasted over 21 days into the withdrawal period. These results suggest that CeA neurons can be a cellular target for cocaine to reshape the circuitry mediating negative affects during withdrawal, and that the long-lasting cellular alterations in selective subpopulations of CeA neurons may lead to unbalanced CeA processing, thus contributing to the progressive aggravation of negative affective states during withdrawal from chronic cocaine exposure."],["dc.identifier.doi","10.1038/npp.2013.124"],["dc.identifier.pmid","23756609"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/84505"],["dc.language.iso","en"],["dc.relation.eissn","1740-634X"],["dc.relation.issn","0893-133X"],["dc.title","Cocaine-induced membrane adaptation in the central nucleus of amygdala"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","E3131"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","E3140"],["dc.bibliographiccitation.volume","112"],["dc.contributor.author","Huang, Xiaojie"],["dc.contributor.author","Stodieck, Sophia Katharina"],["dc.contributor.author","Goetze, Bianka"],["dc.contributor.author","Cui, Lei"],["dc.contributor.author","Wong, Man Ho"],["dc.contributor.author","Wenzel, Colin"],["dc.contributor.author","Hosang, Leon"],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Loewel, Siegrid"],["dc.contributor.author","Schlueter, Oliver M."],["dc.date.accessioned","2018-11-07T09:55:51Z"],["dc.date.available","2018-11-07T09:55:51Z"],["dc.date.issued","2015"],["dc.description.abstract","During critical periods, all cortical neural circuits are refined to optimize their functional properties. The prevailing notion is that the balance between excitation and inhibition determines the onset and closure of critical periods. In contrast, we show that maturation of silent glutamatergic synapses onto principal neurons was sufficient to govern the duration of the critical period for ocular dominance plasticity in the visual cortex of mice. Specifically, postsynaptic density protein-95 (PSD-95) was absolutely required for experience-dependent maturation of silent synapses, and its absence before the onset of critical periods resulted in lifelong juvenile ocular dominance plasticity. Loss of PSD-95 in the visual cortex after the closure of the critical period reinstated silent synapses, resulting in reopening of juvenile-like ocular dominance plasticity. Additionally, silent synapse-based ocular dominance plasticity was largely independent of the inhibitory tone, whose developmental maturation was independent of PSD-95. Moreover, glutamatergic synaptic transmission onto parvalbumin-positive interneurons was unaltered in PSD-95 KO mice. These findings reveal not only that PSD-95-dependent silent synapse maturation in visual cortical principal neurons terminates the critical period for ocular dominance plasticity but also indicate that, in general, once silent synapses are consolidated in any neural circuit, initial experience-dependent functional optimization and critical periods end."],["dc.identifier.doi","10.1073/pnas.1506488112"],["dc.identifier.isi","000356251800009"],["dc.identifier.pmid","26015564"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36839"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Progressive maturation of silent synapses governs the duration of a critical period"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","394"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","408"],["dc.bibliographiccitation.volume","93"],["dc.contributor.author","Liu, Yanling"],["dc.contributor.author","Cui, Lei"],["dc.contributor.author","Schwarz, Martin K."],["dc.contributor.author","Dong, Yan"],["dc.contributor.author","Schlueter, Oliver M."],["dc.date.accessioned","2018-11-07T10:28:21Z"],["dc.date.available","2018-11-07T10:28:21Z"],["dc.date.issued","2017"],["dc.description.abstract","Spike timing-dependent synaptic plasticity (STDP) serves as a key cellular correlate of associative learning, which is facilitated by elevated attentional and emotional states involving activation of adrenergic signaling. At cellular levels, adrenergic signaling increases dendrite excitability, but the underlying mechanisms remain elusive. Here we show that activation of beta 2-adrenoceptors promoted STD long-term synaptic potentiation at mouse hippocampal excitatory synapses by inactivating dendritic Kv1.1-containing potassium channels, which increased dendrite excitability and facilitated dendritic propagation of postsynaptic depolarization, potentially improving coincidental activation of pre- and postsynaptic terminals. We further demonstrate that adrenergic modulation of Kv1.1 was mediated by the signaling scaffold SAP97, which, through direct protein-protein interactions, escorts beta 2 signaling to remove Kv1.1 from the dendrite surface. These results reveal a mechanism through which the postsynaptic signaling scaffolds bridge the aroused brain state to promote induction of synaptic plasticity and potentially to enhance spike timing and memory encoding."],["dc.identifier.doi","10.1016/j.neuron.2016.12.039"],["dc.identifier.isi","000396428200017"],["dc.identifier.pmid","28103480"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43400"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Cell Press"],["dc.relation.issn","1097-4199"],["dc.relation.issn","0896-6273"],["dc.title","Adrenergic Gate Release for Spike Timing-Dependent Synaptic Potentiation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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"]]