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Do the quantitative relationships of synaptic junctions and terminals in the thalamus of genetic absence epilepsy rats from Strasbourg (GAERS) differ from those in normal control Wistar rats

dc.contributor.authorONAT, FİLİZ
dc.contributor.authorsCavdar, Safiye; Hacioglu, Husniye; Dogukan, Secan Y.; Onat, Filiz
dc.date.accessioned2022-03-12T18:06:09Z
dc.date.accessioned2026-01-11T13:55:23Z
dc.date.available2022-03-12T18:06:09Z
dc.date.issued2012
dc.description.abstractAbnormal functional properties of the thalamocortical connections were reported in the absence of epilepsy. The present study compares the ratios of terminals (`RL'-round vesicles, large terminals, 'RS'-round vesicles, small terminals and 'F'-flattened vesicles) and synapse in three first-order (ventrobasal, lateral geniculate and anteroventral) and in three higher-order (posterior, lateral posterior and mediodorsal) thalamic nuclei of genetic absence epilepsy rats from Strasbourg (GAERS) with our earlier quantitative studies of normal Wistar rats to show whether quantitative differences were present in GAERS as compared to Wistar rat. Rats were perfused transcardially, the brains were removed and cut as 300 lmcoronal sections. Parts of the six thalamic nuclei were removed for routine electron microscopy and GABA immunocytochemistry. Twenty photographs from each section at 20,0009 magnification were taken, and the terminals were identified as RL, RS or F. (1) In normal Wistar rats (as in cats), the proportion of driver terminals (RL) and synapses is lower in higherorder than in first-order thalamic nuclei, but this difference is not present in GAERS animals. (2) The proportions of RS terminals and synapses for each thalamic nucleus showed no significant differences between GAERS and Wistar rats for any of the thalamic nuclei. (3) In GAERS, the proportion of inhibitory F terminals and synapses was significantly high in the VB and low in the LP thalamic nucleus. These abnormal ratios in the GAERS may be the cause of the spike-and-wave discharges of absence seizures or may represent a compensatory response of the thalamocortical circuitry to the absence seizures.
dc.identifier.doi10.1007/s10072-011-0666-5
dc.identifier.eissn1590-3478
dc.identifier.issn1590-1874
dc.identifier.pubmed21720899
dc.identifier.urihttps://hdl.handle.net/11424/230848
dc.identifier.wosWOS:000304242100003
dc.language.isoeng
dc.publisherSPRINGER-VERLAG ITALIA SRL
dc.relation.ispartofNEUROLOGICAL SCIENCES
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectElectron microscopy
dc.subjectImmunohistochemistry
dc.subjectThalamus
dc.subjectGABA
dc.subjectDrivers
dc.subjectModulators
dc.subjectLATERAL GENICULATE-NUCLEUS
dc.subjectRETICULAR NUCLEUS
dc.subjectHIGHER-ORDER
dc.subjectWAVE DISCHARGES
dc.subjectPHA-L
dc.subjectCORTICOTHALAMIC PROJECTIONS
dc.subjectGABAERGIC TRANSMISSION
dc.subjectSOMATOSENSORY THALAMUS
dc.subjectRELATIVE DISTRIBUTION
dc.subjectANTEROGRADE TRACER
dc.titleDo the quantitative relationships of synaptic junctions and terminals in the thalamus of genetic absence epilepsy rats from Strasbourg (GAERS) differ from those in normal control Wistar rats
dc.typearticle
dspace.entity.typePublication
oaire.citation.endPage259
oaire.citation.issue2
oaire.citation.startPage251
oaire.citation.titleNEUROLOGICAL SCIENCES
oaire.citation.volume33

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