%0 Journal Article
%T Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils
%A Fang Cao
%A Ryuji Hata
%A Pengxiang Zhu
%A Shoichiro Takeda
%A Tadashi Yoshida
%A Nobuhiro Hakuba
%A Masahiro Sakanaka
%A Kiyofumi Gyo
%J BMC Neuroscience
%D 2010
%I BioMed Central
%R 10.1186/1471-2202-11-115
%X Brainstem ischemia was produced by occlusion of the bilateral vertebral arteries just before their entry into the transverse foramina of the cervical vertebrae of Mongolian gerbils. Animals were subjected to brainstem ischemia for 15 min, and then reperfused for 0 d (just after ischemia), 1 d, 3 d and 7 d (n = 4 in each group). Sham-operated animals (n = 4) were used as control. After deep anesthesia, the gerbils were perfused with fixative for immunohistochemical investigation. Ischemic lesions were detected by immunostaining for microtubule-associated protein 2 (MAP2). Just after 15-min brainstem ischemia, ischemic lesions were detected in the lateral vestibular nucleus and the ventral part of the spinal trigeminal nucleus, and these ischemic lesions disappeared one day after reperfusion in all animals examined. However, 3 days and 7 days after reperfusion, ischemic lesions appeared again and clusters of ionized calcium-binding adapter molecule-1(IBA-1)-positive cells were detected in the same areas in all animals.These results suggest that delayed neuronal cell death took place in the brainstem after transient brainstem ischemia in gerbils.In the central nervous system, certain areas are selectively damaged even after a brief ischemic insult, and this topographical heterogeneity is known as "selective vulnerability of the brain". Hippocampal CA1 and neocortical III, V, and VI are extremely vulnerable to ischemia and hypoxia [1]. The mechanism responsible for this vulnerability is of particular importance to establish therapeutic procedures, because elucidation of the mechanism may lead to the development of novel therapy to ameliorate ischemic damage.Pathologic aspects and the topographic distribution of ischemic lesions after transient ischemia have been extensively studied in the rodent forebrain [2,3]. However, little is known about the distribution of ischemic lesions after transient brainstem ischemia because of the lack of reproducible brainstem ischemia mo
%U http://www.biomedcentral.com/1471-2202/11/115