TY - JOUR
T1 - Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils
AU - Cao, Fang
AU - Hata, Ryuji
AU - Zhu, Pengxiang
AU - Takeda, Shoichiro
AU - Yoshida, Tadashi
AU - Hakuba, Nobuhiro
AU - Sakanaka, Masahiro
AU - Gyo, Kiyofumi
N1 - Funding Information:
This project was supported, in part, by grants from the Ministry of Education, Science, Sports and Culture of Japan. We are grateful for the secretarial assistance of Ms. K. Hiraoka.
PY - 2010/9/14
Y1 - 2010/9/14
N2 - Background: Because of the lack of reproducible brainstem ischemia models in rodents, the temporal profile of ischemic lesions in the brainstem after transient brainstem ischemia has not been evaluated intensively. Previously, we produced a reproducible brainstem ischemia model of Mongolian gerbils. Here, we showed the temporal profile of ischemic lesions after transient brainstem ischemia.Results: 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.Conclusion: These results suggest that delayed neuronal cell death took place in the brainstem after transient brainstem ischemia in gerbils.
AB - Background: Because of the lack of reproducible brainstem ischemia models in rodents, the temporal profile of ischemic lesions in the brainstem after transient brainstem ischemia has not been evaluated intensively. Previously, we produced a reproducible brainstem ischemia model of Mongolian gerbils. Here, we showed the temporal profile of ischemic lesions after transient brainstem ischemia.Results: 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.Conclusion: These results suggest that delayed neuronal cell death took place in the brainstem after transient brainstem ischemia in gerbils.
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U2 - 10.1186/1471-2202-11-115
DO - 10.1186/1471-2202-11-115
M3 - Article
C2 - 20840766
AN - SCOPUS:77956457726
SN - 1471-2202
VL - 11
JO - BMC Neuroscience
JF - BMC Neuroscience
M1 - 115
ER -