Longterm influence of hypoxic-ischemic brain damage in 3-day-old rats on their brain MR imaging and memory and learning ability
10.3760/cma.j.issn.1007-9408.2009.03.013
- VernacularTitle:三日龄大鼠缺氧缺血性脑损伤对大脑MRI影像和学习记忆能力的远期影响
- Author:
Jiangqin LIU
;
Zhiheng HUANG
;
Qingguo WANG
;
Chao CHEN
- Publication Type:Journal Article
- Keywords:
Hypoxia-ischemia,brain;
Infant,premature;
Apoptosis;
Learning;
Memory;
Magnetic resonance imaging
- From:
Chinese Journal of Perinatal Medicine
2009;12(3):205-208
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the activation of apoptotic genes of the brain with hypoxia- ischemia (HI) in newborn SD rats, and MRI changes and memory and learning ability in adulthood. Methods HI was induced by right carotid artery ligation followed by 2.5 h of hypoxia (6% O2) on 3-day-old SD rats (n=36). Control pups were sham-operated (n = 27). Right brain hemisphere was collected at 12 h and 7 d after HI and subjected to an apoptosis Oligo GEArrayR. MRI and Morris water maze test were performed on both groups at 42 and 44 days old, respectively. Results Comparing to 12 h after HI, up-regulated apoptotic genes included TNF, Caspase and pro-apoptotit genes of Bcl2 families, whereas the anti-apoptotic genes of Bcl2 family were down-regulated at 7 d after HI. The MRI assessment of the rats in HI group demonstrated that the area of the right cerebra l cortex was significantly smaller than the left side and control [periventricular layer: (23.5±3.6) mm2 vs (33.0±4.3) mm2, (34.5±3.9) mm2; hippocampus layer: (18.9±4.4) mm2 vs (29.1±5.0) mm2,(30.8±4.5) mm2, both P<0.01]. During the navigation trial, the HI rats demonstrated longer escape latency (4th day: (52.7±35.9) vs (17.8±8. 9) s, P<0.01). HI rats passed the platform less times than the control ones (T= 292.5, P<0.05) in space probe trial. Conclusions The activation of apoptotic genes induced by HI brain injury remains until 7 days later, involving intrinsic and extrinsic apoptotic pathway. The apoptosis of neural cells may lead to poor development of the cortex and impair the memory and learning ability in the adult rats after neonatal hypoxia- ischemia injury.
