Deficits in Spatial Learning and Memory is Associated with Hippocampal Volume Loss in Aged Apolipoprotein E4 Mice

2011 ◽  
Vol 27 (1) ◽  
pp. 89-98 ◽  
Author(s):  
Jun-xiang Yin ◽  
Gregory H. Turner ◽  
Hao-jie Lin ◽  
Stephen W. Coons ◽  
Jiong Shi
2020 ◽  
Author(s):  
YuHang Zhu ◽  
JuanJuan Ren ◽  
Chao Zhang ◽  
TaoWu Gong ◽  
PengCheng Zhao ◽  
...  

Abstract Background: It has been reported that repeated exposure to sevoflurane, a widely used general anesthesia in pediatric surgeries, may lead to brain defect in infant. However, the long-term effect of repeated exposure to sevoflurane during infancy on the learning behavior and neuro-development is less investigated yet.Methods: Sixty-four SD (sprague dawley) rats were randomly divided in to two groups, the experimental group (n=32) was exposed to sevoflurane (2.6%, 2 h) and the control group (n=32) was exposed to carrier gas (1 L/min O2 + 1 L/min Air, 2 h) for three times at infancy (P (postnatal day) 7, P14, and P21). At childhood (P32 to P36), SD rats in each group (n=16) received Morris Water Maze (MWM) test, and then Magnetic Resonance Imaging (MRI) was used to scan their brain and hippocampus at P37. Subsequently, the same NWM test and MRI scanning was conducted for the remaining SD rats in their adulthood (P92 to P97) (n = 16/group).Results: After being exposed to sevoflurane in infancy, the hippocampal volume of SD rats significantly decreased in their childhood and adulthood, their whole brain volume was also shrunken in adulthood; however, MWM test showed there is no obvious change in their spatial learning and memory recall performance either in childhood or in adulthood.Conclusions: Although repeated exposure to sevoflurane in infancy did not affect the spatial learning and memory performance of rats, however, it could result in the decease of hippocampal and brain volume in their adulthood. This study suggests that repetitive sevoflurane exposure in infancy may exert long-term risk in brain development.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Dan Song ◽  
Yaohua Chen ◽  
Cheng Chen ◽  
Lili Chen ◽  
Oumei Cheng

Abstract Purpose and background Previous studies have suggested that promoting endogenous neurogenesis has great significance for the recovery of cognitive dysfunction caused by cerebral ischemia (CI). Pharmacological inhibition of GABAB receptor can enhance neurogenesis in adult healthy and depressed mice. In the study, we intended to investigate the effects of GABAB receptor antagonists on cognitive function and hippocampal neurogenesis in mice following CI. Methods Adult mice were subjected to bilateral common carotid artery occlusion (BCCAO) for 20 min to induce CI and treated with CGP52432 (antagonist of GABAB receptor, CGP, 10 mg/kg intraperitoneal injection) starting 24 h after CI. The Morris water maze test was performed to test spatial learning and memory at day 28. Immunofluorescence was applied to detect neurogenesis in the DG region at day 14 and 28. In in vitro experiments, cell proliferation was detected by CCK8 and immunofluorescence, and the expression of cAMP/CREB signaling pathway-related proteins was detected by ELISA assay and Western blot. Results CGP significantly improved spatial learning and memory disorders caused by CI, and it enhanced the proliferation of neural stem cells (NSCs), the number of immature neurons, and the differentiation from newborn cells to neurons. In vitro experiments further confirmed that CGP dose-dependently enhanced the cell viability of NSCs, and immunofluorescence staining showed that CGP promoted the proliferation of NSCs. In addition, treatment with CGP increased the expression of cAMP, PKA, and pCREB in cultured NSCs. Conclusion Inhibition of GABAB receptor can effectively promote hippocampal neurogenesis and improve spatial learning and memory in adult mice following CI.


Sign in / Sign up

Export Citation Format

Share Document