Histological changes on pyramidal layer of hippocampus following transient cerebral ischemia in gerbils

일시적 대뇌허혈에 의한 gerbil 해마의 피라밋층에 조직학적 변화

  • Yang, Je-hoon (College of Veterinary Medicine, Gyeongsang National University) ;
  • Koh, Phil-ok (College of Veterinary Medicine, Gyeongsang National University) ;
  • Kwak, Soo-dong (Institute of Animal Medicine College of Veterinary Medicine, Gyeongsang National University)
  • 양제훈 (경상대학교 수의과대학) ;
  • 고필옥 (경상대학교 수의과대학) ;
  • 곽수동 (경상대학교 수의과대학 동물의학연구소)
  • Accepted : 2001.11.28
  • Published : 2001.12.24

Abstract

Cardiac arrest, hypoxia, shock or seizure has been known to induce cerebral ischemia. This study was designed to investigate the effect of ischemia on hippocampal pyramidal layer induced by transient bilateral occlusion of the common carotid arteries. Mature Mongolian gerbils were sacrificed at days 2, 4, and 7 after carotid occlusion for 10 minutes. Sham-operated gerbils of control group were subjected to the same protocol except for carotid occlusion. During operation for ischemia, body temperature was maintained $37{\pm}0.5^{\circ}C$ in all gerbils. Paraffin-embedded brain tissue blocks were cut into coronal slices and stained with H-E stain or immunostain by TUNEL method. Neurons with the oval and prominent nucleus and without the eosinophilic cytoplasm in the subfield of hippocamapal pyramidal layer were calculated as to be viable neurons. Their chromatins were condensed or clumped. Their nuclei appeared multiangular or irregularly shrinked. The width of the pyramidal layer was reduced due to the loss of nuclei. At day 2 after reperfusion, some neurons in the CA1 subfield were slightly eosinophilic. But most neurons in the CA2 subfield were strongly eosinophilic. At day 4 day, most neurons in the CA1 subfield were severely damaged and at day 7 day, only a few survived neurons were observed. Survived neurons per longitudinal 1mm sector in the CA1, CA2, CA3, and CA4 subfields of pyramidal layer were investigated. At day 2, the mean numbers of pyramidal neurons in CA1, CA2, CA3, and CA4 subfiedls were 104.5/mm (54.3%), 51.0/mm (33.8%), 105.5/mm (85.6%), and 124.3/mm (93.5%) compared to the nonischemic control group, respectively. At day 4, the mean numbers of pyramidal neurons in CA1, CA2, CA3, and CA4 subfields were 3.2/mm (1.7%), 51.5/mm(34.2%), 95.3/mm (77.4%), and 112.5/mm (84.6%), respectively. At day 7, the mean numbers of pyramidal neurons in CA1, CA2, CA3, and CA4 subfiedls were 0.8/mm (0.4%), 5.7/mm(3.8%), 9.8/mm (8.0%), and 5.0/mm (3.7%), respectively. The mean numbers of apoptotic positive neurons in the CA1 subfield at day 2, 4, and 7 after reperfusion were 67.8/mm, 153.2/mm and 123.7/mm, respectively. These results suggest that the transient cerebral ischemia cause severe damages in most neurons at day 7 and that the prosminent apoptotic positive neurons in hippocampal pyramidal layer are the delayed neuronal death induced by ischemia.