Please use this identifier to cite or link to this item:
http://doi.org/10.25358/openscience-2894Full metadata record
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | Unichenko, Petr | |
| dc.date.accessioned | 2014-10-14T13:56:24Z | |
| dc.date.available | 2014-10-14T15:56:24Z | |
| dc.date.issued | 2014 | |
| dc.identifier.uri | https://openscience.ub.uni-mainz.de/handle/20.500.12030/2896 | - |
| dc.description.abstract | It has been shown in the study that glutamate transporters (EAAT) are capable to modulate GABA transports (GAT). Here we also report that DL-TBOA, a non-transportable glutamate uptake blocker, eliminates GAT-mediated GABA release, while D-aspartate, an EAAT substrate, does not block the latter. The strength or even the operating mode of GABA uptake/release could be influenced by the work of EAATs. Considering the interaction between EAATs and GATs we can conclude that ambient glutamate and GABA levels are mutually dependent. The EAAT-GAT crosstalk observed in this work is mediated by EAAT1 and GAT-2/3. Since both transporters are Na+ dependent and mainly glial, next we investigated the role of [Na+]i in astrocytic-mediated glutamate uptake. We tested whether [Na+]i changes affect paired-pulse plasticity of STCs recorded from cortical layer 2/3 astrocytes. We report that an elevation of [Na+]i induced either by using a high [Na+]i intrapipette solution or by application of GABA slows STCs kinetics and decrease paired-pulse facilitation (PPF) of STCs at short inter-stimulus intervals. Moreover, GAT inhibitors decrease PPF of STCs under control conditions, suggesting that endogenous GABA operating via GATs influences EAAT-mediated transport | en_GB |
| dc.language.iso | eng | |
| dc.rights | InCopyright | de_DE |
| dc.rights.uri | https://rightsstatements.org/vocab/InC/1.0/ | |
| dc.subject.ddc | 570 Biowissenschaften | de_DE |
| dc.subject.ddc | 570 Life sciences | en_GB |
| dc.title | Extracellular glutamate-GABA balance in the developing neocortex | en_GB |
| dc.type | Dissertation | de_DE |
| dc.identifier.urn | urn:nbn:de:hebis:77-38645 | |
| dc.identifier.doi | http://doi.org/10.25358/openscience-2894 | - |
| jgu.type.dinitype | doctoralThesis | |
| jgu.type.version | Original work | en_GB |
| jgu.type.resource | Text | |
| jgu.description.extent | 95 Bl. | |
| jgu.organisation.department | FB 04 Medizin | - |
| jgu.organisation.year | 2014 | |
| jgu.organisation.number | 2700 | - |
| jgu.organisation.name | Johannes Gutenberg-Universität Mainz | - |
| jgu.rights.accessrights | openAccess | - |
| jgu.organisation.place | Mainz | - |
| jgu.subject.ddccode | 570 | |
| opus.date.accessioned | 2014-10-14T13:56:24Z | |
| opus.date.modified | 2014-10-14T14:15:51Z | |
| opus.date.available | 2014-10-14T15:56:24 | |
| opus.subject.dfgcode | 00-000 | |
| opus.organisation.string | FB 04: Medizin: Klinikum | de_DE |
| opus.identifier.opusid | 3864 | |
| opus.institute.number | 0416 | |
| opus.metadataonly | false | |
| opus.type.contenttype | Dissertation | de_DE |
| opus.type.contenttype | Dissertation | en_GB |
| jgu.organisation.ror | https://ror.org/023b0x485 | |
| Appears in collections: | JGU-Publikationen | |
