scholarly journals BAI1 regulates spatial learning and synaptic plasticity in the hippocampus

2015 ◽  
Vol 125 (4) ◽  
pp. 1497-1508 ◽  
Author(s):  
Dan Zhu ◽  
Chenchen Li ◽  
Andrew M. Swanson ◽  
Rosa M. Villalba ◽  
Jidong Guo ◽  
...  
2010 ◽  
Vol 206 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Takahiro Yaguchi ◽  
Tetsu Nagata ◽  
Dongqin Yang ◽  
Tomoyuki Nishizaki

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Zhao-Hui Yao ◽  
Xiao-li Yao ◽  
Shao-feng Zhang ◽  
Ji-chang Hu ◽  
Yong Zhang

Chronic cerebral hypoperfusion (CCH) is a common pathophysiological mechanism that underlies cognitive decline and degenerative processes in dementia and other neurodegenerative diseases. Low cerebral blood flow (CBF) during CCH leads to disturbances in the homeostasis of hemodynamics and energy metabolism, which in turn results in oxidative stress, astroglia overactivation, and synaptic protein downregulation. These events contribute to synaptic plasticity and cognitive dysfunction after CCH. Tripchlorolide (TRC) is an herbal compound with potent neuroprotective effects. The potential of TRC to improve CCH-induced cognitive impairment has not yet been determined. In the current study, we employed behavioral techniques, electrophysiology, Western blotting, immunofluorescence, and Golgi staining to investigate the effect of TRC on spatial learning and memory impairment and on synaptic plasticity changes in rats after CCH. Our findings showed that TRC could rescue CCH-induced spatial learning and memory dysfunction and improve long-term potentiation (LTP) disorders. We also found that TRC could prevent CCH-induced reductions in N-methyl-D-aspartic acid receptor 2B, synapsin I, and postsynaptic density protein 95 levels. Moreover, TRC upregulated cAMP-response element binding protein, which is an important transcription factor for synaptic proteins. TRC also prevented the reduction in dendritic spine density that is caused by CCH. However, sham rats treated with TRC did not show any improvement in cognition. Because CCH causes disturbances in brain energy homeostasis, TRC therapy may resolve this instability by correcting a variety of cognitive-related signaling pathways. However, for the normal brain, TRC treatment led to neither disturbance nor improvement in neural plasticity. Additionally, this treatment neither impaired nor further improved cognition. In conclusion, we found that TRC can improve spatial learning and memory, enhance synaptic plasticity, upregulate the expression of some synaptic proteins, and increase the density of dendritic spines. Our findings suggest that TRC may be beneficial in the treatment of cognitive impairment induced by CCH.


2019 ◽  
Vol 9 (9) ◽  
pp. 236 ◽  
Author(s):  
Xue Li ◽  
Lu Wang ◽  
Shuling Zhang ◽  
Xiang Hu ◽  
Huijun Yang ◽  
...  

This study was designed to investigate beneficial effects of swimming exercise training on learning/memory, synaptic plasticity and CREB (cAMP response element binding protein) expression in hippocampus in a rat model of d-galactose-induced aging (DGA). Eighty adult male rats were randomly divided into four groups: Saline Control (group C), DGA (group A), Swimming exercise before DGA (group S1), and Swimming during DGA (group S2). These four groups of animals were further divided into Morris water maze training group (M subgroup) and sedentary control group (N subgroup). Spatial learning/memory was tested using Morris water maze training. The number and density of synaptophysin (Syp) and metabotropic glutamate receptor 1 (mGluR1) in hippocampal dentate gyrus area, CREB mRNA and protein expression and DNA methylation levels were determined respectively with immunohistochemistry, western blot, real-time PCR, and MassArray methylation detection platform. We found that compared with group C, DGA rats showed aging-like poor health and weight loss as well as hippocampal neurodegenerative characteristics. Exercise training led to a time-dependent decrease in average escape latency and improved spatial memory. Exercise training group (S2M) had significantly increased swim distance as compared with controls. These functional improvements in S2M group were associated with higher Syp and mGluR1 values in hippocampus (p < 0.01) as well as higher levels of hippocampal CREB protein/mRNA expression and gene methylation. In conclusion, swimming exercise training selectively during drug-induced aging process protected hippocampal neurons against DGA-elicited degenerative changes and in turn maintained neuronal synaptic plasticity and learning/memory function, possibly through upregulation of hippocampal CREB protein/mRNA and reduction of DGA-induced methylation of CREB.


2015 ◽  
Vol 1621 ◽  
pp. 170-186 ◽  
Author(s):  
Nicole Sabaliauskas ◽  
Hui Shen ◽  
Jonela Molla ◽  
Qi Hua Gong ◽  
Aarti Kuver ◽  
...  

2014 ◽  
Vol 7 (1) ◽  
Author(s):  
Jun-Hyeok Choi ◽  
Pojeong Park ◽  
Gi-Chul Baek ◽  
Su-Eon Sim ◽  
SukJae Joshua Kang ◽  
...  

Neurosignals ◽  
2011 ◽  
Vol 20 (1) ◽  
pp. 1-14 ◽  
Author(s):  
Francisco J. Monje ◽  
Eun-Jung Kim ◽  
Daniela D. Pollak ◽  
Maureen Cabatic ◽  
Lin Li ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document