mycoreobjectrosdok_disshab_0000000091rosdok_disshab_0000000091rosdokdisshabrosdok_derivate_00000036002023-08-08T10:00:19.418Z2008-10-02T16:07:44.736Zadministratorpublished1rosdok_derivate_0000003600truetruederivate_types:fulltextVolltextfulltextwf_edit_epub wf_register_epubstate:publishedstate:publishedveröffentlichtpublishedrosdok/id00000351578811413MODS updated during RosDok migration in June 2021DissertationHochschulschrift136349730Josef AaronAvshalomov1975-VerfasserInautThe role of NMDA receptor subunits in the regulation of synaptic plasticity in dorsomedial striatum in a model of paroxysmal dystoniaenProf. Dr.RüdigerKöhlingAkademischeR BetreuerIndgsProf. Dr.DieterWeissAkademischeR BetreuerIndgs2147083-2Universität RostockMathematisch-Naturwissenschaftliche FakultätGrad-verleihende Institutiondgg10.18453/rosdok_id00000351http://purl.uni-rostock.de/rosdok/id00000351urn:nbn:de:gbv:28-diss2008-0085-5570 Biowissenschaften, BiologieMathematisch-Naturwissenschaftliche Fakultätfrei zugänglich (Open Access)Lizenz Metadaten: CC0Nutzungsrechte erteiltalle Rechte vorbehaltenUniversität RostockRostock2007monographic20082007Universitätsbibliothek RostockRostock20082008Dystonias are movement disorders whose pathomechanism is largely unknown. The dtsz dystonic hamster mutant represents a model of primary paroxysmal dystonia, where alterations of striatal interneuron density and long term potentiation were described (Köhling et al., 2004, Gernert et al., 2000). In the present thesis, using corticostriatal slices, we explore in more detail whether long-term potentiation (LTP) and long-term depression (LTD) are shifted by a) behavioural stimulation or b) ontogenetic maturation using different stimulation protocols in the cortico-striatal synaptic pathway. The third aim of the thesis was c) to explore the role of NMDA receptors and their subunits in synaptic plasticity changes occurring with dystonia. Field extracellular recordings were conducted in dorsomedial striatum, and white matter was stimulated. Short and long term plasticity as well as input-output relationships were analysed. The main findings were: a. The occurrence of enhanced synaptic plasticity is not dependent on behavioural stimulation, while changes in excitability are. b. Ontogenetic maturation increases the dynamic range of synaptic plasticity under normal conditions, which is infringed in animals with dystonia, even though the symptoms have remitted. c. In dystonic tissue, LTP is dependent on NR2A, wheras in normal tissue, it depends on NR2B receptors. In conclusion, the functional shifts in NR2A vs. NR2B involvement in synaptic corticostriatal plasticity may be instrumental in the pathogenesis of dystonia in the dtsz model.synaptic plasticitystriatumdystonic hamstersUniversitätsbibliothek Rostockhttp://purl.uni-rostock.de/rosdok/id00000351doctype:epubdoctype:epubDokumenttypDocument typedoctype:epub.dissertationdoctype:epub.dissertationDissertationdoctoral thesisdiniPublType:doctoralThesis diniPublType2022:PhDThesis XMetaDissPlusThesisLevel:thesis.doctoralinfo:eu-repo/semantics/doctoralThesisdocumentnatureOfContent:ppn_105825778natureOfContent:ppn_105825778HochschulschriftdiniPublType2022:DoctoralThesisdiniPublType2022:DoctoralThesisDissertation oder HabilitationDoctoral thesisDRIVERdiniPublType2022:PhDThesisdiniPublType2022:PhDThesisDissertationPhD thesisKDSF (Pu34)XMetaDissPlusThesisLevel:thesis.doctoralXMetaDissPlusThesisLevel:thesis.doctoralDoktorarbeitdoctoral thesisrfc5646:enrfc5646:enEnglischEnglishengengSDNB:570SDNB:570570 Biowissenschaften, Biologie570 Life scienceinstitution:unirostockinstitution:unirostockUniversität RostockUniversity of RostockUniversität RostockUniversität RostockUni.Rostockhttp://d-nb.info/gnd/38329-6institution:unirostock.mnfinstitution:unirostock.mnfMathematisch-Naturwissenschaftliche FakultätFaculty of Mathematics and Natural SciencesUniversität Rostock. Mathematisch-Naturwissenschaftliche FakultätMathematisch-Natur-<br />wissenschaftliche FakultätUni.Rostock.Fakultaet.MNFhttp://d-nb.info/gnd/2147083-2accesscondition:openaccessaccesscondition:openaccessfrei zugänglich (Open Access)open accesshttp://purl.org/coar/access_right/c_abf2OAfreeinfo:eu-repo/semantics/openAccess[DE-28]Open Access$gControlled Vocabulary for Access Rights$uhttp://purl.org/coar/access_right/c_abf2licenseinfo:metadatalicenseinfo:metadataLizenzen für Metadatenlicenseinfo:metadata.cc0licenseinfo:metadata.cc0Lizenz Metadaten: CC0license metadata: CC0/creativecommons/p/zero/1.0/88x31.pnghttps://creativecommons.org/publicdomain/zero/1.0/licenseinfo:depositlicenseinfo:depositVeröffentlichungsgenehmigungpermission to storelicenseinfo:deposit.rightsgrantedlicenseinfo:deposit.rightsgrantedNutzungsrechte erteiltrights grantedlicenseinfo:worklicenseinfo:workWerkworklicenseinfo:work.rightsreservedlicenseinfo:work.rightsreservedalle Rechte vorbehaltenall rights reserved/creativecommons/r/reserved/0.9/88x31.png[DE-28]Urheberrechtsschutz 1.0$gRights Statements$uhttp://rightsstatements.org/vocab/InC/1.0/http://rightsstatements.org/vocab/InC/1.0/http://rightsstatements.org/vocab/InC/1.0/The role of NMDA receptor subunits in the regulation of synaptic plasticity in dorsomedial striatum in a model of paroxysmal dystoniaThe role of NMDA receptor subunits in the regulation of synaptic plasticity in dorsomedial striatum in a model of paroxysmal dystoniagnd:136349730gnd:2147083-2gnd:136349730gnd:2147083-2rosdok_disshab_0000000091-d3009784e39gnd:136349730Josef Aaron AvshalomovJosef Aaron Avshalomovrosdok_disshab_0000000091-d3009784e60Prof. Dr. Rüdiger KöhlingProf. Dr. Rüdiger Köhlingrosdok_disshab_0000000091-d3009784e72Prof. Dr. Dieter WeissProf. Dr. Dieter Weissrosdok_disshab_0000000091-d3009784e84gnd:2147083-2Universität Rostock Mathematisch-Naturwissenschaftliche FakultätUniversität Rostock Mathematisch-Naturwissenschaftliche FakultätJosef Aaron AvshalomovProf. Dr. Rüdiger KöhlingProf. Dr. Dieter WeissUniversität Rostock Mathematisch-Naturwissenschaftliche FakultätJosef Aaron AvshalomovProf. Dr. Rüdiger KöhlingProf. Dr. Dieter WeissUniversität Rostock Mathematisch-Naturwissenschaftliche FakultätJosef Aaron AvshalomovRostockUniversität Rostockepub.dissertation10.18453/rosdok_id00000351http://purl.uni-rostock.de/rosdok/id00000351urn:nbn:de:gbv:28-diss2008-0085-5synaptic plasticitystriatumdystonic hamstersDystonias are movement disorders whose pathomechanism is largely unknown. The dtsz dystonic hamster mutant represents a model of primary paroxysmal dystonia, where alterations of striatal interneuron density and long term potentiation were described (Köhling et al., 2004, Gernert et al., 2000). In the present thesis, using corticostriatal slices, we explore in more detail whether long-term potentiation (LTP) and long-term depression (LTD) are shifted by a) behavioural stimulation or b) ontogenetic maturation using different stimulation protocols in the cortico-striatal synaptic pathway. The third aim of the thesis was c) to explore the role of NMDA receptors and their subunits in synaptic plasticity changes occurring with dystonia. Field extracellular recordings were conducted in dorsomedial striatum, and white matter was stimulated. Short and long term plasticity as well as input-output relationships were analysed. The main findings were: a. The occurrence of enhanced synaptic plasticity is not dependent on behavioural stimulation, while changes in excitability are. b. Ontogenetic maturation increases the dynamic range of synaptic plasticity under normal conditions, which is infringed in animals with dystonia, even though the symptoms have remitted. c. In dystonic tissue, LTP is dependent on NR2A, wheras in normal tissue, it depends on NR2B receptors. In conclusion, the functional shifts in NR2A vs. NR2B involvement in synaptic corticostriatal plasticity may be instrumental in the pathogenesis of dystonia in the dtsz model.20072007epub.dissertation1 Dissertation_Avshalomov_2008.pdf 1393627 f1a4b4977b670d8e3dcfe8715d99b658 rosdok/id00000351578811413MODS updated during RosDok migration in June 2021DissertationHochschulschrift136349730Josef AaronAvshalomov1975-VerfasserInautThe role of NMDA receptor subunits in the regulation of synaptic plasticity in dorsomedial striatum in a model of paroxysmal dystoniaenProf. Dr.RüdigerKöhlingAkademischeR BetreuerIndgsProf. Dr.DieterWeissAkademischeR BetreuerIndgs2147083-2Universität RostockMathematisch-Naturwissenschaftliche FakultätGrad-verleihende Institutiondgg10.18453/rosdok_id00000351http://purl.uni-rostock.de/rosdok/id00000351urn:nbn:de:gbv:28-diss2008-0085-5570 Biowissenschaften, BiologieMathematisch-Naturwissenschaftliche Fakultätfrei zugänglich (Open Access)Lizenz Metadaten: CC0Nutzungsrechte erteiltalle Rechte vorbehaltenUniversität RostockRostock2007monographic20082007Universitätsbibliothek RostockRostock20082008Dystonias are movement disorders whose pathomechanism is largely unknown. The dtsz dystonic hamster mutant represents a model of primary paroxysmal dystonia, where alterations of striatal interneuron density and long term potentiation were described (Köhling et al., 2004, Gernert et al., 2000). In the present thesis, using corticostriatal slices, we explore in more detail whether long-term potentiation (LTP) and long-term depression (LTD) are shifted by a) behavioural stimulation or b) ontogenetic maturation using different stimulation protocols in the cortico-striatal synaptic pathway. The third aim of the thesis was c) to explore the role of NMDA receptors and their subunits in synaptic plasticity changes occurring with dystonia. Field extracellular recordings were conducted in dorsomedial striatum, and white matter was stimulated. Short and long term plasticity as well as input-output relationships were analysed. The main findings were: a. The occurrence of enhanced synaptic plasticity is not dependent on behavioural stimulation, while changes in excitability are. b. Ontogenetic maturation increases the dynamic range of synaptic plasticity under normal conditions, which is infringed in animals with dystonia, even though the symptoms have remitted. c. In dystonic tissue, LTP is dependent on NR2A, wheras in normal tissue, it depends on NR2B receptors. In conclusion, the functional shifts in NR2A vs. NR2B involvement in synaptic corticostriatal plasticity may be instrumental in the pathogenesis of dystonia in the dtsz model.synaptic plasticitystriatumdystonic hamstersUniversitätsbibliothek Rostockhttp://purl.uni-rostock.de/rosdok/id00000351 2008-10-02T16:07:44.736Z 2023-08-08T10:00:19.418Z 2023-08-18T10:00:19.422Z {"identifier":"rosdok/id00000351","type":"local_id","additional":"","service":"MCRLocalID","created":"2018-06-30T12:33:29.851Z"} {"identifier":"http://purl.uni-rostock.de/rosdok/id00000351","type":"purl","additional":"","service":"RosDokPURL","created":"2018-06-30T12:33:30.048Z","registered":"2018-06-30T12:33:30.048Z"} {"identifier":"10.18453/rosdok_id00000351","type":"doi","additional":"","service":"RosDokDOI","created":"2018-06-30T12:33:31.493Z","registered":"2018-06-30T12:33:31.493Z"} {"identifier":"urn:nbn:de:gbv:28-diss2008-0085-5","type":"dnbUrn","additional":"","service":"RosDokURN","created":"2018-06-30T12:33:29.855Z","registered":"2008-10-06T02:14:21.430Z"} administratorfulltextfile/rosdok_disshab_0000000091/rosdok_derivate_0000003600/Dissertation_Avshalomov_2008.pdfThe role of NMDA receptor subunits in the regulation of synaptic plasticity in dorsomedial striatum in a model of paroxysmal dystoniaThe role of NMDA receptor subunits in the regulation of synaptic plasticity in dorsomedial striatum in a model of paroxysmal dystoniagnd:136349730gnd:2147083-2gnd:136349730gnd:2147083-2rosdok_disshab_0000000091-d3009784e39gnd:136349730Josef Aaron AvshalomovJosef Aaron Avshalomovrosdok_disshab_0000000091-d3009784e60Prof. Dr. Rüdiger KöhlingProf. Dr. Rüdiger Köhlingrosdok_disshab_0000000091-d3009784e72Prof. Dr. Dieter WeissProf. Dr. Dieter Weissrosdok_disshab_0000000091-d3009784e84gnd:2147083-2Universität Rostock Mathematisch-Naturwissenschaftliche FakultätUniversität Rostock Mathematisch-Naturwissenschaftliche FakultätJosef Aaron AvshalomovProf. Dr. Rüdiger KöhlingProf. Dr. Dieter WeissUniversität Rostock Mathematisch-Naturwissenschaftliche FakultätJosef Aaron AvshalomovProf. Dr. Rüdiger KöhlingProf. Dr. Dieter WeissUniversität Rostock Mathematisch-Naturwissenschaftliche FakultätJosef Aaron AvshalomovRostockUniversität Rostockepub.dissertation10.18453/rosdok_id00000351http://purl.uni-rostock.de/rosdok/id00000351urn:nbn:de:gbv:28-diss2008-0085-5synaptic plasticitystriatumdystonic hamstersDystonias are movement disorders whose pathomechanism is largely unknown. The dtsz dystonic hamster mutant represents a model of primary paroxysmal dystonia, where alterations of striatal interneuron density and long term potentiation were described (Köhling et al., 2004, Gernert et al., 2000). In the present thesis, using corticostriatal slices, we explore in more detail whether long-term potentiation (LTP) and long-term depression (LTD) are shifted by a) behavioural stimulation or b) ontogenetic maturation using different stimulation protocols in the cortico-striatal synaptic pathway. The third aim of the thesis was c) to explore the role of NMDA receptors and their subunits in synaptic plasticity changes occurring with dystonia. Field extracellular recordings were conducted in dorsomedial striatum, and white matter was stimulated. Short and long term plasticity as well as input-output relationships were analysed. The main findings were: a. The occurrence of enhanced synaptic plasticity is not dependent on behavioural stimulation, while changes in excitability are. b. Ontogenetic maturation increases the dynamic range of synaptic plasticity under normal conditions, which is infringed in animals with dystonia, even though the symptoms have remitted. c. In dystonic tissue, LTP is dependent on NR2A, wheras in normal tissue, it depends on NR2B receptors. In conclusion, the functional shifts in NR2A vs. NR2B involvement in synaptic corticostriatal plasticity may be instrumental in the pathogenesis of dystonia in the dtsz model.20072007[xslt]Saxonrosdok/id00000351https://purl.uni-rostock.de/rosdok/id0000035157881141310.18453/rosdok_id00000351urn:nbn:de:gbv:28-diss2008-0085-5Josef Aaron AvshalomovAvshalomov Josef AaronThe role of NMDA receptor subunits in the regulation of synaptic plasticity in dorsomedial striatum in a model of paroxysmal dystoniaDissertationdoctoral thesisUniversität Rostock, 2007Dystonias are movement disorders whose pathomechanism is largely unknown. The dtsz dystonic hamster mutant represents a model of primary paroxysmal dystonia, where alterations of striatal interneuron density and long term potentiation were described (Köhling et al., 2004, Gernert et al., 2000). In…Josef Aaron AvshalomovThe role of NMDA receptor subunits in the regulation of synaptic plasticity in dorsomedial striatum in a model of paroxysmal dystoniaUniversitätsbibliothek Rostockhttp://purl.uni-rostock.de/rosdok/id00000351136349730Josef AaronAvshalomov1975-VerfasserInautProf. Dr.RüdigerKöhlingAkademischeR BetreuerIndgsProf. Dr.DieterWeissAkademischeR BetreuerIndgs2147083-2Universität RostockMathematisch-Naturwissenschaftliche FakultätGrad-verleihende Institutiondgg[doi]10.18453/rosdok_id00000351[purl]http://purl.uni-rostock.de/rosdok/id00000351[urn]urn:nbn:de:gbv:28-diss2008-0085-5open_access20072007epoch:21th_centuryrfc5646:endoctype:epub.dissertationaccesscondition:openaccessSDNB:570institution:unirostock.mnfstate:published