Medrihan, Lucian

[["dc.bibliographiccitation.firstpage","2915"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","2930"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Kobe, Fritz"],["dc.contributor.author","Guseva, Daria"],["dc.contributor.author","Jensen, Thomas P."],["dc.contributor.author","Wirth, Alexander"],["dc.contributor.author","Renner, Ute"],["dc.contributor.author","Hess, Dietmar"],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Medrihan, Lucian"],["dc.contributor.author","Zhang, Weiqi"],["dc.contributor.author","Zhang, Mingyue"],["dc.contributor.author","Braun, Katharina"],["dc.contributor.author","Westerholz, Sören"],["dc.contributor.author","Herzog, Andreas"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Richter, Diethelm W."],["dc.contributor.author","Rusakov, Dmitri A."],["dc.contributor.author","Ponimaskin, Evgeni"],["dc.date.accessioned","2017-09-07T11:46:22Z"],["dc.date.available","2017-09-07T11:46:22Z"],["dc.date.issued","2012"],["dc.description.abstract","The common neurotransmitter serotonin controls different aspects of early neuronal differentiation, although the underlying mechanisms are poorly understood. Here we report that activation of the serotonin 5-HT7 receptor promotes synaptogenesis and enhances synaptic activity in hippocampal neurons at early postnatal stages. An analysis of Gα12-deficient mice reveals a critical role of G12-protein for 5-HT7 receptor-mediated effects in neurons. In organotypic preparations from the hippocampus of juvenile mice, stimulation of 5-HT7R/G12 signaling potentiates formation of dendritic spines, increases neuronal excitability, and modulates synaptic plasticity. In contrast, in older neuronal preparations, morphogenetic and synaptogenic effects of 5-HT7/G12 signaling are abolished. Moreover, inhibition of 5-HT7 receptor had no effect on synaptic plasticity in hippocampus of adult animals. Expression analysis reveals that the production of 5-HT7 and Gα12-proteins in the hippocampus undergoes strong regulation with a pronounced transient increase during early postnatal stages. Thus, regulated expression of 5-HT7 receptor and Gα12-protein may represent a molecular mechanism by which serotonin specifically modulates formation of initial neuronal networks during early postnatal development."],["dc.identifier.doi","10.1523/JNEUROSCI.2765-11.2012"],["dc.identifier.gro","3150488"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7258"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.title","5-HT₇R/G₁₂ signaling regulates neuronal morphology and function in an age-dependent manner"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","jcs.182089"],["dc.bibliographiccitation.journal","Journal of Cell Science"],["dc.contributor.author","Valente, Pierluigi"],["dc.contributor.author","Lignani, Gabriele"],["dc.contributor.author","Medrihan, Lucian"],["dc.contributor.author","Bosco, Federica"],["dc.contributor.author","Contestabile, Andrea"],["dc.contributor.author","Lippiello, Pellegrino"],["dc.contributor.author","Ferrea, Enrico"],["dc.contributor.author","Schachner, Melitta"],["dc.contributor.author","Benfenati, Fabio"],["dc.contributor.author","Giovedì, Silvia"],["dc.contributor.author","Baldelli, Pietro"],["dc.date.accessioned","2022-10-06T13:26:14Z"],["dc.date.available","2022-10-06T13:26:14Z"],["dc.date.issued","2016"],["dc.description.abstract","L1 is a trans-membrane glycoprotein subserving neuron-neuron adhesion via homophilic and heterophilic interactions. Although experimental evidences have implicated L1 in axonal outgrowth, fasciculation and pathfinding, its contribution to voltage-gated sodium channels (NaChs) function and membrane excitability has remained unknown. Here, we show that firing rate, single cell spiking frequency and Na+ current density are all reduced in hippocampal excitatory neurons from L1-deficient mice both in culture and in slices, due to an overall reduced membrane expression of NaChs.\n Remarkably, normal firing activity was restored when L1 was reintroduced into L1-deficient excitatory neurons, indicating that abnormal firing patterns are not related to developmental abnormalities, but are a direct consequence of L1 deletion. Moreover, L1-deficiency leads to impairment of action potential (AP) initiation, most likely due to the loss of the interaction of L1 with Ankyrin G that produces the delocalization of NaChs at the at the axonal initial segment. We conclude that L1 contributes to functional expression and localization of NaChs to the neuronal plasma membrane, ensuring correct initiation of AP and normal firing activity."],["dc.identifier.doi","10.1242/jcs.182089"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/115033"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.eissn","1477-9137"],["dc.relation.issn","0021-9533"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Cell adhesion molecule L1 contributes to neuronal excitability regulating the function of voltage-gated sodium channels"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5095"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","The Journal of Physiology"],["dc.bibliographiccitation.lastpage","5106"],["dc.bibliographiccitation.volume","587"],["dc.contributor.author","Medrihan, Lucian"],["dc.contributor.author","Rohlmann, Astrid"],["dc.contributor.author","Fairless, Richard"],["dc.contributor.author","Andrae, Johanna"],["dc.contributor.author","Doring, Markus"],["dc.contributor.author","Missler, Markus"],["dc.contributor.author","Zhang, W."],["dc.contributor.author","Kilimann, Manfred W."],["dc.date.accessioned","2018-11-07T11:22:55Z"],["dc.date.available","2018-11-07T11:22:55Z"],["dc.date.issued","2009"],["dc.description.abstract","The development of neuronal networks in the brain requires the differentiation of functional synapses. Neurobeachin (Nbea) was identified as a putative regulator of membrane protein trafficking associated with tubulovesicular endomembranes and postsynaptic plasma membranes. Nbea is essential for evoked transmission at neuromuscular junctions, but its role in the central nervous system has not been characterized. Here, we have studied central synapses of a newly generated gene-trap knockout (KO) mouse line at embryonic day 18, because null-mutant mice are paralysed and die perinatally. Although the overall brain architecture was normal, we identified major abnormalities of synaptic function in mutant animals. In acute slices from the brainstem, both spontaneous excitatory and inhibitory postsynaptic currents were clearly reduced and failure rates of evoked inhibitory responses were markedly increased. In addition, the frequency of miniature excitatory and both the frequency and amplitudes of miniature inhibitory postsynaptic currents were severely diminished in KO mice, indicating a perturbation of both action potential-dependent and -independent transmitter release. Moreover, Nbea appears to be important for the formation and composition of central synapses because the area density of mature asymmetric contacts in the fetal brainstem was reduced to 30% of wild-type levels, and the expression levels of a subset of synaptic marker proteins were smaller than in littermate controls. Our data demonstrate for the first time a function of Nbea at central synapses that may be based on its presumed role in targeting membrane proteins to synaptic contacts, and are consistent with the 'excitatory-inhibitory imbalance' model of autism where Nbea gene rearrangements have been detected in some patients."],["dc.identifier.doi","10.1113/jphysiol.2009.178236"],["dc.identifier.isi","000271416900016"],["dc.identifier.pmid","19723784"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56077"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.relation.issn","0022-3751"],["dc.title","Neurobeachin, a protein implicated in membrane protein traffic and autism, is required for the formation and functioning of central synapses"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","37"],["dc.bibliographiccitation.journal","BMC Biology"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Adamcio, Bartosz"],["dc.contributor.author","Sargin, Derya"],["dc.contributor.author","Stradomska, Alicja"],["dc.contributor.author","Medrihan, Lucian"],["dc.contributor.author","Gertler, Christoph"],["dc.contributor.author","Theis, Fabian"],["dc.contributor.author","Zhang, Mingyue"],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Hassouna, Imam"],["dc.contributor.author","Hannke, Kathrin"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Schulze, Lizzy"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Wolf, Fred"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Rhee, Jeong-Seop"],["dc.contributor.author","Zhang, Weiqi"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:48:12Z"],["dc.date.available","2017-09-07T11:48:12Z"],["dc.date.issued","2008"],["dc.description.abstract","Background: Erythropoietin (EPO) improves cognition of human subjects in the clinical setting by as yet unknown mechanisms. We developed a mouse model of robust cognitive improvement by EPO to obtain the first clues of how EPO influences cognition, and how it may act on hippocampal neurons to modulate plasticity. Results: We show here that a 3-week treatment of young mice with EPO enhances long-term potentiation (LTP), a cellular correlate of learning processes in the CAI region of the hippocampus. This treatment concomitantly alters short-term synaptic plasticity and synaptic transmission, shifting the balance of excitatory and inhibitory activity. These effects are accompanied by an improvement of hippocampus dependent memory, persisting for 3 weeks after termination of EPO injections, and are independent of changes in hematocrit. Networks of EPO-treated primary hippocampal neurons develop lower overall spiking activity but enhanced bursting in discrete neuronal assemblies. At the level of developing single neurons, EPO treatment reduces the typical increase in excitatory synaptic transmission without changing the number of synaptic boutons, consistent with prolonged functional silencing of synapses. Conclusion: We conclude that EPO improves hippocampus dependent memory by modulating plasticity, synaptic connectivity and activity of memory-related neuronal networks. These mechanisms of action of EPO have to be further exploited for treating neuropsychiatric diseases."],["dc.identifier.doi","10.1186/1741-7007-6-37"],["dc.identifier.gro","3143237"],["dc.identifier.isi","000260109300001"],["dc.identifier.pmid","18782446"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8430"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/729"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1741-7007"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Erythropoietin enhances hippocampal long-term potentiation and memory"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","112"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neurophysiology"],["dc.bibliographiccitation.lastpage","121"],["dc.bibliographiccitation.volume","99"],["dc.contributor.author","Medrihan, Lucian"],["dc.contributor.author","Tantalaki, Evangelia"],["dc.contributor.author","Aramuni, Gayane"],["dc.contributor.author","Sargsyan, Vardanush"],["dc.contributor.author","Dudanova, Irina"],["dc.contributor.author","Missler, Markus"],["dc.contributor.author","Zhang, W."],["dc.date.accessioned","2018-11-07T11:20:15Z"],["dc.date.available","2018-11-07T11:20:15Z"],["dc.date.issued","2008"],["dc.description.abstract","Rett syndrome is a neurodevelopmental disorder caused by mutations in the transcriptional repressor methyl-CpG- binding protein 2 (MeCP2) and represents the leading genetic cause for mental retardation in girls. MeCP2-mutant mice have been generated to study the molecular mechanisms of the disease. It was suggested that an imbalance between excitatory and inhibitory neurotransmission is responsible for the behavioral abnormalities, although it remained largely unclear which synaptic components are affected and how cellular impairments relate to the time course of the disease. Here, we report that MeCP2 KO mice present an imbalance between inhibitory and excitatory synaptic transmission in the ventrolateral medulla already at postnatal day 7. Focusing on the inhibitory synaptic transmission we show that GABAergic, but not glycinergic, synaptic transmission is strongly depressed in MeCP2 KO mice. These alterations are presumably due to both decreased presynaptic gamma-aminobutyric acid (GABA) release with reduced levels of the vesicular inhibitory transmitter transporter and reduced levels of postsynaptic GABA(A)-receptor subunits alpha 2 and alpha 4. Our data indicate that in the MeCP2 -/y mice specific synaptic molecules and signaling pathways are impaired in the brain stem during early postnatal development. These observations mandate the search for more refined diagnostic tools and may provide a rationale for the timing of future therapeutic interventions in Rett patients."],["dc.identifier.doi","10.1152/jn.00826.2007"],["dc.identifier.isi","000252398500010"],["dc.identifier.pmid","18032561"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55490"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Physiological Soc"],["dc.relation.issn","0022-3077"],["dc.title","Early defects of GABAergic synapses in the brain stem of a MeCP2 mouse model of Rett syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]