El-Kordi, Ahmed

[["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.firstpage","41"],["dc.bibliographiccitation.journal","Behavioural Brain Research"],["dc.bibliographiccitation.lastpage","49"],["dc.bibliographiccitation.volume","251"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Winkler, Daniela"],["dc.contributor.author","Hammerschmidt, Kurt"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Krueger, Dilja"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Ritter, Caroline"],["dc.contributor.author","Jatho, Jasmin"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","Bourgeron, Thomas"],["dc.contributor.author","Fischer, Julia"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:47:38Z"],["dc.date.available","2017-09-07T11:47:38Z"],["dc.date.issued","2013"],["dc.description.abstract","Autism is the short name of a complex and heterogeneous group of disorders (autism spectrum disorders, ASD) with several lead symptoms required for classification, including compromised social interaction, reduced verbal communication and stereotyped repetitive behaviors/restricted interests. The etiology of ASD is still unknown in most cases but monogenic heritable forms exist that have provided insights into ASD pathogenesis and have led to the notion of autism as a 'synapse disorder'. Among the most frequent monogenic causes of autism are loss-of-function mutations of the NLGN4X gene which encodes the synaptic cell adhesion protein neuroligin-4X (NLGN4X). We previously described autism-like behaviors in male Nlgn4 null mutant mice, including reduced social interaction and ultrasonic communication. Here, we extend the phenotypical characterization of Nlgn4 null mutant mice to both genders and add a series of additional autism-relevant behavioral readouts. We now report similar social interaction and ultrasonic communication deficits in females as in males. Furthermore, aggression, nest-building parameters, as well as self-grooming and circling as indicators of repetitive behaviors/stereotypies were explored in both genders. The construction of a gender-specific autism severity composite score for Nlgn4 mutant mice markedly diminishes population/sample heterogeneity typically obtained for single tests, resulting in p values of <0.00001 and a genotype predictability of 100% for male and of >83% for female mice. Taken together, these data underscore the similarity of phenotypical consequences of Nlgn4/NLGN4X loss-of-function in mouse and man, and emphasize the high relevance of Nlgn4 null mutant mice as an ASD model with both construct and face validity."],["dc.identifier.doi","10.1016/j.bbr.2012.11.016"],["dc.identifier.gro","3142307"],["dc.identifier.isi","000322927700006"],["dc.identifier.pmid","23183221"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6831"],["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","0166-4328"],["dc.subject","Social interaction; Nest building; Grooming; Repetitive behaviors; Stereotypies; Ultra-sound vocalization; Gender differences; ASD"],["dc.title","Development of an autism severity score for mice using Nlgn4 null mutants as a construct-valid model of heritable monogenic autism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","592"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Genes, Brain and Behavior"],["dc.bibliographiccitation.lastpage","602"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Castaneda, S."],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Reim, Kerstin"],["dc.contributor.author","Bickeböller, H."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Brose, N."],["dc.contributor.author","Ehrenreich, Hanhelore"],["dc.date.accessioned","2017-09-07T11:45:21Z"],["dc.date.available","2017-09-07T11:45:21Z"],["dc.date.issued","2010"],["dc.description.abstract","Schizophrenia is a devastating disease that affects approximately 1% of the population across cultures. Its neurobiological underpinnings are still unknown. Accordingly, animal models of schizophrenia often lack construct validity. As concordance rate in monozygotic twins amounts to only 50%, environmental risk factors (e.g. neurotrauma, drug abuse, psychotrauma) likely act as necessary 'second hit' to trigger/drive the disease process in a genetically predisposed individual. Valid animal models would have to consider this genetic-environmental interaction. Based on this concept, we designed an experimental approach for modeling a schizophrenia-like phenotype in mice. As dysfunction in synaptic transmission plays a key role in schizophrenia, and complexin2 (CPLX2) gene expression is reduced in hippocampus of schizophrenic patients, we developed a mouse model with Cplx2 null mutation as genetic risk factor and a mild parietal neurotrauma, applied during puberty, as environmental 'second hit'. Several months after lesion, Cplx2 null mutants showed reduced pre-pulse inhibition, deficit of spatial learning and loss of inhibition after MK-801 challenge. These abnormalities were largely absent in lesioned wild-type mice and non-lesioned Cplx2 null mutants. Forced alternation in T-maze, object recognition, social interaction and elevated plus maze tests were unaltered in all groups. The previously reported mild motor phenotype of Cplx2 null mutants was accentuated upon lesion. MRI volumetrical analysis showed a decrease of hippocampal volume exclusively in lesioned Cplx2 null mutants. These findings provide suggestive evidence for the 'second hit' hypothesis of schizophrenia and may offer new tools for the development of advanced treatment strategies."],["dc.identifier.doi","10.1111/j.1601-183X.2010.00590.x"],["dc.identifier.gro","3142880"],["dc.identifier.isi","000281032700005"],["dc.identifier.pmid","20412316"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/332"],["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","1601-1848"],["dc.title","Complexin2 null mutation requires a 'second hit' for induction of phenotypic changes relevant to schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1352"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Cell Science"],["dc.bibliographiccitation.lastpage","1361"],["dc.bibliographiccitation.volume","122"],["dc.contributor.author","Reim, Kerstin"],["dc.contributor.author","Regus-Leidig, Hanna"],["dc.contributor.author","Ammermueller, Josef"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Brandstaetter, Johann Helmut"],["dc.contributor.author","Brose, Nils"],["dc.date.accessioned","2017-09-07T11:47:29Z"],["dc.date.available","2017-09-07T11:47:29Z"],["dc.date.issued","2009"],["dc.description.abstract","Complexins regulate the speed and Ca(²⁺) sensitivity of SNARE-mediated synaptic vesicle fusion at conventional synapses. Two of the vertebrate complexins, Cplx3 and Cplx4, are specifically localized to retinal ribbon synapses. To test whether Cplx3 and Cplx4 contribute to the highly efficient transmitter release at ribbon synapses, we studied retina function and structure in Cplx3 and Cplx4 single- and double-knockout mice. Electroretinographic recordings from single and double mutants revealed a cooperative perturbing effect of Cplx3 and Cplx4 deletion on the b-wave amplitude, whereas most other detected effects in both plexiform synaptic layers were additive. Light and electron microscopic analyses uncovered a disorganized outer plexiform layer in the retinae of mice lacking Cplx3 and Cplx4, with a significant proportion of photoreceptor terminals containing spherical free-floating ribbons. These structural and functional aberrations were accompanied by behavioural deficits indicative of a vision deficit. Our results show that Cplx3 and Cplx4 are essential regulators of transmitter release at retinal ribbon synapses. Their loss leads to aberrant adjustment and fine-tuning of transmitter release at the photoreceptor ribbon synapse, alterations in transmission at bipolar cell terminals, changes in the temporal structure of synaptic processing in the inner plexiform layer of the retina and perturbed vision."],["dc.identifier.doi","10.1242/jcs.045401"],["dc.identifier.gro","3143119"],["dc.identifier.isi","000265443300011"],["dc.identifier.pmid","19386896"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/598"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: German Research Foundation [SFB523/B9, FOR701/TP7, BR 1643/4-1]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0021-9533"],["dc.title","Aberrant function and structure of retinal ribbon synapses in the absence of complexin 3 and complexin 4"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","337"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","Schizophrenia Research"],["dc.bibliographiccitation.lastpage","338"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Klaus, Sabrina"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Malzahn, Dörthe"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","Benseler, Fritz"],["dc.contributor.author","Reim, Kerstin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2022-03-01T11:45:23Z"],["dc.date.available","2022-03-01T11:45:23Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1016/j.schres.2010.02.583"],["dc.identifier.pii","S0920996410006687"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103308"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0920-9964"],["dc.title","Complexin2 Gene Polymorphisms Modify Cognitive Performance in Schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]