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dc.contributor.authorBerggaard, Nina
dc.contributor.authorWitter, Menno
dc.contributor.authorvan der Want, Johannes Jacobus Leendert
dc.identifier.citationFrontiers in Systems Neuroscience. 2019, 13:10 1-8.nb_NO
dc.description.abstractLayer II of the medial entorhinal cortex (MEC LII) contains the largest number of spatially modulated grid cells and is one of the first regions in the brain to express Alzheimer’s disease (AD)-related pathology. The most common principal cell type in MEC LII, reelin-expressing stellate cells, are grid cell candidates. Recently we found evidence that γ-aminobutyric acid (GABA)A receptor subunits show a specific distribution in MEC LII, in which GABAA α3 is selectively associated with reelin-positive neurons, with limited association with the other principal cell type, calbindin (CB)-positive pyramidal neurons. Furthermore, the expression of α3 subunit decreases in mice between P15 and P25, which coincides with the emergence of stable grid cell activity. It has been shown that the α3 subunit undergoes specific developmental changes and that it may exert pro-inflammatory actions if improperly regulated. In this review article, we evaluate the changing kinetics of α3-GABAA receptors (GABAARs). during development in relation to α3-subunit expression pattern in MEC LII and conclude that α3 could be closely related to the stabilization of grid cell activity and theta oscillations. We further conclude that dysregulated α3 may be a driving factor in early AD pathology.nb_NO
dc.publisherFrontiers Medianb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleGABAA receptor subunit α3 in network dynamics in the medial entorhinal cortexnb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.source.journalFrontiers in Systems Neurosciencenb_NO
dc.description.localcodeCopyright © 2019 Berggaard, Witter and van der Want. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms .nb_NO
cristin.unitnameInstitutt for klinisk og molekylær medisin
cristin.unitnameKavliinstitutt for nevrovitenskap

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Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal