Radulovic, Jelena

[["dc.bibliographiccitation.firstpage","786"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neuron"],["dc.bibliographiccitation.lastpage","798"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Schrick, Christina"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Srivastava, Deepak P."],["dc.contributor.author","Tronson, Natalie C."],["dc.contributor.author","Penzes, Peter"],["dc.contributor.author","Radulovic, Jelena"],["dc.date.accessioned","2017-09-07T11:49:25Z"],["dc.date.available","2017-09-07T11:49:25Z"],["dc.date.issued","2007"],["dc.description.abstract","Cadherin-mediated interactions are integral to synapse formation and potentiation. Here we show that N-cadherin is required for memory formation and regulation of a subset of underlying biochemical processes. N-cadherin antagonistic peptide containing the His-Ala-Val motif (HAV-N) transiently disrupted hippocampal N-cadherin dimerization and impaired the formation of long-term contextual fear memory while sparing short-term memory, retrieval, and extinction. HAV-N impaired the learning-induced phosphorylation of a distinctive, cytoskeletally associated fraction of hippocampal Erk-1/2 and altered the distribution of IQGAP1, a scaffold protein linking cadherin-mediated cell adhesion to the cytoskeleton. This effect was accompanied by reduction of N-cadherin/ IQGAP1/Erk-2 interactions. Similarly, in primary neuronal cultures, HAV-N prevented NMDA-induced dendritic Erk-1/2 phosphorylation and caused relocation of IQGAP1 from dendritic spines into the shafts. The data suggest that the newly identified role of hippocampal N-cadherin in memory consolidation may be mediated, at least in part, by cytoskeletal IQGAP1/Erk signaling."],["dc.identifier.doi","10.1016/j.neuron.2007.07.034"],["dc.identifier.gro","3143441"],["dc.identifier.isi","000249857000014"],["dc.identifier.pmid","17785185"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/955"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: NIMH NIH HHS [R01 MH073669, R01 MH073669-02]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0896-6273"],["dc.title","N-cadherin regulates cytoskeletally associated lQGAP1/ERK signaling and memory formation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","463"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Molecular and Cellular Neuroscience"],["dc.bibliographiccitation.lastpage","476"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Schrick, Christina"],["dc.contributor.author","Spiess, Joachim"],["dc.contributor.author","Radulovic, Jelena"],["dc.date.accessioned","2017-09-07T11:45:13Z"],["dc.date.available","2017-09-07T11:45:13Z"],["dc.date.issued","2002"],["dc.description.abstract","The phosphorylation of proteins involved in the MAP kinase signal transduction pathway was investigated during associative learning of C57BL/6J mice. Context-dependent fear conditioning, consisting of a single exposure of mice to a context followed by foot shock, was employed as a learning paradigm. Control groups consisted of mice exposed to context only or an immediate shock in the context. Coincident up-regulation of phosphorylated Erk-1/2 and Elk-1 was observed in the CA3 hippocampal subfield and dentate gyrus 30 min after fear conditioning but not after the control paradigms. Phosphorylated Erk-1/2 and Elk-1 were associated and predominantly colocalized in the mossy fibers. In vitro kinase assays showed that hippocampal Erk-1/2 phosphorylates Elk-1. Notably, Elk-1 in turn enhances the phosphorylation of Erk-1/2 and its downstream target p90Rsk-1. Increased phosphorylation and nuclear translocation of p90Rsk-1 was also demonstrated in the CA3 hippocampal area in vivo during contextual fear conditioning. The observed interactions between hippocampal Elk-1 and Erk-1/2 proteins may affect the consolidation of contextual memories through activation of the downstream nuclear targets of Erk-1/2, such as p90Rsk-1, without requiring nuclear translocation of Elk-1 and Erk-1/2."],["dc.identifier.doi","10.1006/mcne.2002.1188"],["dc.identifier.gro","3144158"],["dc.identifier.isi","000180054800008"],["dc.identifier.pmid","12498787"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1751"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1044-7431"],["dc.title","Phosphorylation of hippocampal Erk-1/2, Elk-1, and p90-Rsk-1 during contextual fear conditioning: Interactions between Erk-1/2 and Elk-1"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1962"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","1966"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Schrick, Christina"],["dc.contributor.author","Spiess, Joachim"],["dc.contributor.author","Radulovic, Jelena"],["dc.date.accessioned","2017-09-07T11:43:59Z"],["dc.date.available","2017-09-07T11:43:59Z"],["dc.date.issued","2004"],["dc.description.abstract","It is believed that de novo protein synthesis is fundamentally linked to synaptic changes in neuronal circuits involved in acquisition and extinction of conditioned responses. Recent studies show that neuronal plasticity may be also altered by cytoskeletal rearrangement independently of protein synthesis. We investigated the role of these processes in the hippocampus during acquisition and extinction of context-dependent conditioned fear in mice. Intrahippocampal injections of the protein synthesis inhibitors anisomycin and puromycin, or of the actin rearrangement inhibitors cytochalasin D and latrunculin A, prevented the acquisition of context-dependent fear. Unexpectedly, anisomycin and puromycin enhanced extinction without erasing the fear memory. In contrast, cytochalasin D and latrunculin A prevented extinction of context-dependent freezing. On the basis of these findings, it is suggested that certain hippocampal mechanisms mediating extinction of conditioned contextual fear are inhibited by protein synthesis and involve actin rearrangement. Such mechanisms might predominantly elicit modifications of hippocampal circuits that store the conditioning memory."],["dc.identifier.doi","10.1523/JNEUROSCI.5112-03.2004"],["dc.identifier.gro","3144009"],["dc.identifier.isi","000189210300020"],["dc.identifier.pmid","14985438"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1586"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.title","Distinct roles of hippocampal de novo protein synthesis and actin rearrangement in extinction of contextual fear"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3700"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","The Journal of neuroscience"],["dc.bibliographiccitation.lastpage","3707"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Schrick, Christina"],["dc.contributor.author","Spiess, Joachim"],["dc.contributor.author","Radulovic, Jelena"],["dc.date.accessioned","2017-09-07T11:45:54Z"],["dc.date.available","2017-09-07T11:45:54Z"],["dc.date.issued","2002"],["dc.description.abstract","Transient stressful experiences may persistently facilitate associative and nonassociative learning, possibly through alterations of gene expression. Here we identify, by subtractive hybridization, differential expression of the Cdk5 gene in response to stress. The Cdk5 protein is selectively induced in the fibers of septohippocampal cholinergic neurons but not in other regions of prominent Cdk5 production. This upregulation is accompanied by increased Cdk5 kinase activity, which is blocked completely by the Cdk5 inhibitor butyrolactone I. Microinjection of butyrolactone I into the lateral septum and hippocampus prevents the acquisition of conditioned context-dependent fear as well as its stress-induced facilitation. By demonstrating that a transient increase of Cdk5 activity within the septohippocampal system is required for associative learning, an important novel role of Cdk5 has been identified."],["dc.identifier.doi","10.1523/JNEUROSCI.22-09-03700.2002"],["dc.identifier.gro","3144203"],["dc.identifier.isi","000175296200047"],["dc.identifier.pmid","11978846"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1802"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0270-6474"],["dc.title","Cyclin-dependent kinase 5 is required for associative learning"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1089"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Neuropharmacology"],["dc.bibliographiccitation.lastpage","1099"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Fischer, André"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Schrick, Christina"],["dc.contributor.author","Spiess, Joachim"],["dc.contributor.author","Radulovic, Jelena"],["dc.date.accessioned","2021-06-01T10:50:06Z"],["dc.date.available","2021-06-01T10:50:06Z"],["dc.date.issued","2003"],["dc.description.abstract","In this work, we confirm the novel role of cyclin-dependent kinase (Cdk) 5 in associative learning by demonstrating that injection of the Cdk5 inhibitor butyrolactone I into the lateral septum or hippocampus profoundly impaired context-dependent fear conditioning of C57BL/6J mice. However, unlike the inducible up regulation of Cdk5 and its regulator p35 observed in Balb/c mice, high baseline levels, which were not affected by fear conditioning, were found in C57BL/6J mice. Surprisingly, microinjections of butyrolactone I into the lateral septum or hippocampus significantly decreased baseline Cdk5 activity within the entire septohippocampal circuitry, suggesting a functional link between septal and hippocampal Cdk5 activity. Significantly higher levels of the transcription factor Sp4 in the septo-hippocampal system of C57BL/6J mice may account for the high baseline Cdk5/p35 production. On the other hand, the stronger cFos production observed in the lateral septum of fear conditioned Balb/c mice may be responsible, at least in part, for the inducible up-regulation of Cdk5 in this strain. These results suggest that the role of Cdk5 in memory consolidation is strain independent and functionally related to the septo-hippocampal circuitry. However, the molecular regulation of baseline and inducible Cdk5 protein might be different among individual mouse strains and possibly other species."],["dc.identifier.doi","10.1016/S0028-3908(03)00102-3"],["dc.identifier.gro","3144104"],["dc.identifier.isi","000183374900011"],["dc.identifier.pmid","12763101"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86532"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0028-3908"],["dc.title","Regulation of contextual fear conditioning by baseline and inducible septo-hippocampal cyclin-dependent kinase 5"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","149"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurobiology of Learning and Memory"],["dc.bibliographiccitation.lastpage","158"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Radulovic, Marko"],["dc.contributor.author","Schrick, Christina"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Godovac-Zimmermann, Jasminka"],["dc.contributor.author","Radulovic, Jelena"],["dc.date.accessioned","2017-09-07T11:49:53Z"],["dc.date.available","2017-09-07T11:49:53Z"],["dc.date.issued","2007"],["dc.description.abstract","Fear memories elicit multiple behavioral responses, encompassing avoidance, or behavioral inhibition in response to threatening contexts. Context-specific freezing, reflecting fear-induced behavioral inhibition, has been proposed as one of the main risks factors for the development of anxiety disorders. We attempted to define the key hippocampal mediators of extinction in a mouse model of contextdependent freezing. Nine-week-old male C57BL/6J mice were trained and tested for contextual fear conditioning and extinction. Freezing behavior scored by unbiased sampling, was used as an index of fear. Proteomic, immunoblot, and immunohistochemical approaches were employed to identify, verify, and analyze the alterations of the hippocampal extracellular signal-regulated kinases 1 and 2 (Erk-1/2). Targeted pharmacological inhibition of the Erk-1/2 activating kinase, the mitogen activated and extracellular signal-regulated kinase (Mek), served to establish the role of Nlek/Erk signaling in extinction. When compared to acquisition, extinction of contextual freezing triggered a rapid activation of Erk-1/2 showing a distinctive time-course, nuclear localization, and subcellular isoform distribution. These differences suggested that the upstream regulation and downstream effects of this pathway might be specific for each process. Dorsohippocampat injections of the Mek inhibitors U0126 (0.5 mu g/site) and PD98059 (1.5 mu g/site) immediately after the nonreinforced trials prevented Erk-1/2 activation and significantly impaired extinction. This effect was dissociable from potential actions on memory retrieval or reconsolidation. On the basis of these findings, we propose that hippocampal Mek/Erk signaling might serve as one of the key mediators of contextual fear extinction."],["dc.identifier.doi","10.1016/j.nlm.2006.08.003"],["dc.identifier.gro","3143565"],["dc.identifier.isi","000243643400016"],["dc.identifier.pmid","16979915"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1093"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: NIMH NIH HHS [MH073669, R01 MH073669]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1074-7427"],["dc.title","Hippocampal Mek/Erk signaling mediates extinction of contextual freezing behavior"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","707"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Neuropharmacology"],["dc.bibliographiccitation.lastpage","710"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Radulovic, Jelena"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Katerkamp, Ulrike"],["dc.contributor.author","Spiess, Joachim"],["dc.date.accessioned","2021-06-01T10:50:06Z"],["dc.date.available","2021-06-01T10:50:06Z"],["dc.date.issued","2000"],["dc.description.abstract","We have demonstrated previously that stimulation of hippocampal corticotropin-releasing factor (CRF) receptors enhances, whereas stimulation of CRF receptors in the lateral intermediate septum impairs learning, as indicated by fear conditioning. Here, we report that the action of CRF within the hippocampus and lateral septum require muscarinic and D2 receptors, respectively. (C) 2000 Elsevier Science Ltd. All rights reserved."],["dc.identifier.doi","10.1016/S0028-3908(99)00185-9"],["dc.identifier.gro","3144426"],["dc.identifier.isi","000085517600019"],["dc.identifier.pmid","10728892"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86533"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Pergamon-elsevier Science Ltd"],["dc.relation.issn","0028-3908"],["dc.title","Role of regional neurotransmitter receptors in corticotropin-releasing factor (CRF)-mediated modulation of fear conditioning"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","200"],["dc.bibliographiccitation.issue","4-5"],["dc.bibliographiccitation.journal","Neurosignals"],["dc.bibliographiccitation.lastpage","208"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Spiess, Joachim"],["dc.contributor.author","Radulovic, Jelena"],["dc.date.accessioned","2017-09-07T11:45:06Z"],["dc.date.available","2017-09-07T11:45:06Z"],["dc.date.issued","2003"],["dc.description.abstract","Learning and memory are processes by which organisms acquire, retain and retrieve information. They result in modifications of behavior in response to new or previously encountered stimuli thereby enabling adaptation to a permanently changing environment. Protein phosphorylation has long been known to play a key role in triggering synaptic changes underlying learning and memory. Although intracellular phosphorylation and dephosphorylation is orchestrated by a complex network of interactions between a number of protein kinases and phosphatases, significant advances in the understanding of neuronal mechanisms underlying learning and memory have been achieved by investigating the actions of individual molecules under defined experimental conditions, brain areas, neuronal cells and their subcellular compartments. On the basis of these approaches, the cyclic AMP protein kinase (PKA), protein kinase C (PKC) and extracellularly regulated protein kinases 1 and 2 (Erk-1/2) have been identified as the core signaling pathways in memory consolidation. Here we review recent findings demonstrating an important novel role for Cdk5 in learning and memory. We suggest that some of the well-characterized roles of Cdk5 during neurodevelopmental processes, such as interactions with distinct cytoplasmic and synaptic target molecules, may be also involved in synaptic plasticity underlying memory consolidation within the adult central nervous system."],["dc.identifier.doi","10.1159/000074621"],["dc.identifier.gro","3144143"],["dc.identifier.isi","000187210600006"],["dc.identifier.pmid","14673206"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1735"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1424-862X"],["dc.title","Cdk5: A novel role in learning and memory"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1012"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","1019"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Wang, Xinyu"],["dc.contributor.author","Schrick, Christina"],["dc.contributor.author","Neve, Rachael"],["dc.contributor.author","Radulovic, Jelena"],["dc.contributor.author","Tsai, Li-Huei"],["dc.date.accessioned","2017-09-07T11:49:26Z"],["dc.date.available","2017-09-07T11:49:26Z"],["dc.date.issued","2007"],["dc.description.abstract","Treatment of emotional disorders involves the promotion of extinction processes, which are defined as the learned reduction of fear. The molecular mechanisms underlying extinction have only begun to be elucidated. By employing genetic and pharmacological approaches in mice, we show here that extinction requires downregulation of Rac-1 and cyclin-dependent kinase 5 (Cdk5), and upregulation of p21 activated kinase-1 (PAK-1) activity. This is physiologically achieved by a Rac-1-dependent relocation of the Cdk5 activator p35 from the membrane to the cytosol and dissociation of p35 from PAK-1. Moreover, our data suggest that Cdk5/p35 activity prevents extinction in part by inhibition of PAK-1 activity in a Rac-1-dependent manner. We propose that extinction of contextual fear is regulated by counteracting components of a molecular pathway involving Rac-1, Cdk5 and PAK-1. Our data suggest that this pathway could provide a suitable target for therapeutic treatment of emotional disorders."],["dc.identifier.doi","10.1038/nn1943"],["dc.identifier.gro","3143461"],["dc.identifier.isi","000248357500015"],["dc.identifier.pmid","17632506"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/977"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1097-6256"],["dc.title","A hippocampal Cdk5 pathway regulates extinction of contextual fear"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1570"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","1583"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Tronson, Natalie C."],["dc.contributor.author","Schrick, Christina"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Sananbenesi, Farahnaz"],["dc.contributor.author","Pages, Gilles"],["dc.contributor.author","Pouyssegur, Jacques"],["dc.contributor.author","Radulovic, Jelena"],["dc.date.accessioned","2017-09-07T11:48:17Z"],["dc.date.available","2017-09-07T11:48:17Z"],["dc.date.issued","2008"],["dc.description.abstract","Human anxiety is frequently accompanied by depression, and when they co-occur both conditions exhibit greater severity and resistance to treatment. Little is known, however, about the molecular processes linking these emotional and mood disorders. Based on previously reported phosphorylation patterns of extracellular signal-regulated kinase (ERK) in the brain, we hypothesized that ERK's upstream activators intertwine fear and mood regulation through their hippocampal actions. We tested this hypothesis by studying the upstream regulation of ERK signaling in behavioral models of fear and depression. Wild-type and ERK1-deficient mice were used to study the dorsohippocampal actions of the putative ERK activators: mitogen-activated and extracellular signal-regulated kinase (MEK), protein kinase C (PKC), and cAMP-dependent protein kinase (PKA). Mice lacking ERK1 exhibited enhanced fear extinction and reduced depression caused by overactivation of ERK2. Both behaviors were reversed by inhibition of MEK, however the extinction phenotype depended on hippocampal, whereas the depression phenotype predominantly involved extrahippocampal MEK. Unexpectedly, inhibition of PKC accelerated extinction and decreased depression by ERK-independent mechanisms, whereas inhibition of PKA did not produce detectable molecular or behavioral effects in the employed paradigm. These results indicate that, contrary to fear conditioning but similar to mood stabilization, extinction of fear required upregulation of MEK/ERK and downregulation of ERK-independent PKC signaling. The dissociation of these pathways may thus represent a common mechanism for fear and mood regulation, and a potential therapeutic option for comorbid anxiety and depression."],["dc.identifier.doi","10.1038/sj.npp.1301550"],["dc.identifier.gro","3143289"],["dc.identifier.isi","000255897700008"],["dc.identifier.pmid","17712345"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/786"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: NIMH NIH HHS [R01 MH073669-02, R01 MH073669, MH073669]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0893-133X"],["dc.title","Regulatory mechanisms of fear extinction and depression-like behavior"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]