Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils
1 Department of Functional Histology, Ehime University Graduate School of Medicine, Shitsukawa, Toon, Ehime 791-0295, Japan
2 Department of Otolaryngology, Ehime University Graduate School of Medicine, Shitsukawa, Toon-shi, Ehime 791-0295, Japan
BMC Neuroscience 2010, 11:115 doi:10.1186/1471-2202-11-115Published: 14 September 2010
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.
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.