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Calretinin immunoreactivity in focal cortical dysplasias and in non-malformed epileptic cortex
Filip Barinka, Rastislav Druga, Petr Marusic, Pavel Krsek, Josef Zamecnik
Jazyk angličtina Země Nizozemsko
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NR8843
MZ0
CEP - Centrální evidence projektů
NS9915
MZ0
CEP - Centrální evidence projektů
- MeSH
- dítě MeSH
- dospělí MeSH
- elektroencefalografie MeSH
- epilepsie metabolismus patologie MeSH
- fluorodeoxyglukosa F18 diagnostické užití MeSH
- hipokampus metabolismus patologie MeSH
- interneurony metabolismus MeSH
- lidé středního věku MeSH
- lidé MeSH
- magnetická rezonanční tomografie MeSH
- malformace mozkové kůry patologie MeSH
- mladiství MeSH
- mladý dospělý MeSH
- mozková kůra metabolismus patologie MeSH
- parvalbuminy metabolismus MeSH
- pozitronová emisní tomografie MeSH
- předškolní dítě MeSH
- S100 kalcium vázající protein G metabolismus MeSH
- Check Tag
- dítě MeSH
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladiství MeSH
- mladý dospělý MeSH
- mužské pohlaví MeSH
- předškolní dítě MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Focal cortical dysplasias (FCDs) represent a prominent cause of pharmacologically intractable epilepsy. In FCD, the decrease of parvalbumin immunoreactive (PV+) inhibitory interneurons has been repeatedly documented. Here, we wanted to show whether another interneuronal population, the calretinin immunoreactive (CR+) neurons, exhibits any change in human FCD. We also investigated samples of morphologically normal temporal neocortex resected together with sclerotic hippocampus (nHSTN), where decrease of PV+ interneurons was previously documented as well. Brain tissue from 24 patients surgically treated for pharmacoresistant epilepsy was examined. Calretinin immunoreactivity was qualitatively evaluated and the density of CR+ neuronal profiles was quantified. As a control, post-mortem acquired neocortical samples of nine patients without any brain affecting disease were used. CR+ neurons were located predominantly in superficial cortical layers both in controls and pathological samples. Similarly, the morphology of CR+ neurons was unaffected in pathological samples. The overall density of CR+ neurons was significantly decreased in FCD type I (to approximately 70% of control values) and even more in FCD type II (to approximately 50% of controls). In nHSTN, no change compared to controls was found in CR+ neuronal density. Our results may contribute to the better understanding of the role of individual interneuronal populations in epileptogenesis.
Department of Anatomy Charles University Prague 1st Faculty of Medicine Prague Czech Republic
Department of Anatomy Charles University Prague 2nd Faculty of Medicine Prague Czech Republic
Department of Anatomy Charles University Prague Czech Republic
Department of Neurology Charles University Prague 2nd Faculty of Medicine Prague Czech Republic
Department of Neurosurgery Charles University Prague 1st Faculty of Medicine Prague Czech Republic
Citace poskytuje Crossref.org
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- $a Barinka, Filip. $7 _AN052438 $u Department of Anatomy, Charles University in Prague, Czech Republic. filipbarinka@yahoo.co.uk
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- $a Focal cortical dysplasias (FCDs) represent a prominent cause of pharmacologically intractable epilepsy. In FCD, the decrease of parvalbumin immunoreactive (PV+) inhibitory interneurons has been repeatedly documented. Here, we wanted to show whether another interneuronal population, the calretinin immunoreactive (CR+) neurons, exhibits any change in human FCD. We also investigated samples of morphologically normal temporal neocortex resected together with sclerotic hippocampus (nHSTN), where decrease of PV+ interneurons was previously documented as well. Brain tissue from 24 patients surgically treated for pharmacoresistant epilepsy was examined. Calretinin immunoreactivity was qualitatively evaluated and the density of CR+ neuronal profiles was quantified. As a control, post-mortem acquired neocortical samples of nine patients without any brain affecting disease were used. CR+ neurons were located predominantly in superficial cortical layers both in controls and pathological samples. Similarly, the morphology of CR+ neurons was unaffected in pathological samples. The overall density of CR+ neurons was significantly decreased in FCD type I (to approximately 70% of control values) and even more in FCD type II (to approximately 50% of controls). In nHSTN, no change compared to controls was found in CR+ neuronal density. Our results may contribute to the better understanding of the role of individual interneuronal populations in epileptogenesis.
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- $a Druga, Rastislav, $d 1940- $7 nlk19990073109 $u Department of Anatomy, Charles University in Prague, 2nd Faculty of Medicine, Prague, Czech Republic; Department of Anatomy, Charles University in Prague, 1st Faculty of Medicine, Prague, Czech Republic
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