作者: Lori A. Mudrick , Kenneth G. Baimbridge
DOI: 10.1016/0006-8993(89)91014-7
关键词: Hippocampus 、 Biology 、 Parvalbumin 、 Central nervous system 、 Ischemia 、 Hippocampal formation 、 Calbindin 、 Pathology 、 Immunostaining 、 GABAergic
摘要: Histological and immunohistochemical techniques were used to investigate the long-term structural changes that occur in rat hippocampal formation following induction of transient forebrain ischemia. analysis showed after 6–12 months cell loss was still largely restricted CA1 region but within this degeneration progressive culminated a severe shrinkage stratum oriens radiatum. Using markers calbindin-D38K parvalbumin, we able demonstrate some reflect shrinkage. Calbindin immunohistochemistry clearly illustrated primarily due pyramidal neurons framework normally provided by their long apical dendrites. Parvalbumin immunostaining demonstrated although few GABAergic interneurons survived insult, terminal network reduced greatly dendrites which extended length radiatum retracted. Additionally, dense band parvalbumin immunoreactivity lacunosum-moleculare, thought be indicative fiber bundle travelling through region, almost completely depleted. These data illustrate primary damage observed cerebral ischemia is not static may thus have important functional implications.