"0"^^ . "7"^^ . . "Damage of interneurons within the hippocampus and dentate gyrus after status epilepticus in developing rats"@en . "7"^^ . "Po\u0161kozen\u00ED interneuron\u016F v hipokampu a gyrus dentatus po status epilepticus u ml\u00E1\u010Fat potkan\u016F" . . . "\u0158ada prac\u00ED dokazuje, \u017Ee nezral\u00FD hipokampus je odoln\u00FD k\u00A0po\u0161kozen\u00ED epileptick\u00FDmi z\u00E1chvaty. Tyto z\u00E1v\u011Bry jsou d\u011Bl\u00E1ny na z\u00E1klad\u011B anal\u00FDzy pole CA3 (obvykle v\u00A0jedin\u00E9m \u010Dasov\u00E9m intervalu), proto jsme se rozhodli pomoc\u00ED FluoroJade B (FJB) studovat morfologick\u00E9 zm\u011B"@cs . . . . . . . "GA304/04/0464" . "Temporal lobe epilepsy represents majority of therapy-resistant epilepsies in patients. Many cases start during childhood. This epilepsy is characterized morphologically by hippocampanal sclerosis affecting mostly dentate gyrus and hippocampal fields CA 1 and CA 3. Similar neuropathological damage was reported in experimental models of status epilepticus. Description of these changes was usually restricted to principal cells in adult animals whereas more that 10 different subpopulations of inhibitory interneurons were neglected. Damage of these interneurons may represent an important factor in epileptogenesis. Aim of this project is to describe localization of hippocampal neurons degenerating after status epilepticus in immature rats with attention focused on interneurons and to characterize these cells by means of double staining (FluoroJade B and calcium-binding proteins). Temporal sequence of morphological changes might help to find the most vulnerable neurons whose death may start the whole"@en . "Neuvedeno."@en . . . "2007-10-16+02:00"^^ . . . "http://www.isvav.cz/projectDetail.do?rowId=GA304/04/0464"^^ . . "0"^^ . . . . "Some published data conclude that immature hippocampus is resistant to seizure-induced damage. These conclusions are usually based on examination of the part of hippocampal formation where damage was described in adult rats (CA3 field) and at only one ti"@en . "1"^^ . . . "Tempol\u00E1rn\u00ED epilepsie maj\u00ED nejv\u011Bt\u0161\u00ED pod\u00EDl na epilepsi\u00EDch rezistentn\u00EDch na farmakoterapii. Zna\u010Dn\u00E1 \u010D\u00E1st t\u011Bchto epilepsi\u00ED za\u010D\u00EDn\u00E1 ji\u017E v d\u011Btstv\u00ED. Jejich morfologick\u00FDm korel\u00E1tem je obvykle mesiotempor\u00E1ln\u00ED skler\u00F3za postihuj\u00EDc\u00ED gyrus dentatus a hipokampov\u00E9 sektory CA1 a CA3. Podobn\u00E9 zm\u011Bny jsou pops\u00E1ny u experiment\u00E1ln\u00EDch model\u016F status epilepticus, popis je v\u0161ak obvykle omezen jen na pyramidov\u00E9 \u010Di granul\u00E1rn\u00ED bu\u0148ky u dosp\u011Bl\u00FDch zv\u00ED\u0159at, inhibi\u010Dn\u00ED interneurony, kter\u00FDch je v hipokampov\u00E9 formaci v\u00EDce ne\u017E 10typ\u016F, z\u016Fst\u00E1vaj\u00ED stranou pozornosti. Po\u0161kozen\u00ED t\u011Bchto element\u016F m\u016F\u017Ee p\u0159edstavovat d\u016Fle\u017Eit\u00FD faktor v epileptogeneze. Proto budeme studovat u ml\u00E1\u010Fat potkan\u016F lokalizaci inhibi\u010Dn\u00EDch neuron\u016F degeneruj\u00EDc\u00EDch po epileptick\u00E9m statu a budeme je charakterizovat pomoc\u00ED dvoj\u00EDho zna\u010Den\u00ED (FluoroJade B a kalcium-v\u00E1\u017E\u00EDc\u00ED proteiny). \u010Casov\u00FD sled morfologick\u00FDch zm\u011Bn umo\u017En\u00ED vytypovat bu\u0148ky, kter\u00E9 jsou nejzraniteln\u011Bj\u0161\u00ED a pravd\u011Bpodobn\u011B stoj\u00ED na za\u010D\u00E1tku cel\u00E9 kask\u00E1dy hipokampov\u00E9ho po\u0161kozen\u00ED. Progresivn\u00ED zm\u011Bny, kter\u00E9 jsou reakc\u00ED na" . . .