Escitalopram Ameliorates Tau Hyperphosphorylation and Spatial Memory Deficits Induced by Protein Kinase A Activation in Sprague Dawley Rats

2015 ◽  
Vol 47 (1) ◽  
pp. 61-71 ◽  
Author(s):  
Qing-Guo Ren ◽  
Yan-Juan Wang ◽  
Wei-Gang Gong ◽  
Lin Xu ◽  
Zhi-Jun Zhang
2004 ◽  
Vol 151 (1-2) ◽  
pp. 287-293 ◽  
Author(s):  
Yu-Wen Huang ◽  
Wei-Wei Hu ◽  
Zhong Chen ◽  
Li-San Zhang ◽  
Hai-Qing Shen ◽  
...  

Hippocampus ◽  
2009 ◽  
Vol 19 (1) ◽  
pp. 90-98 ◽  
Author(s):  
Berta Sunyer ◽  
Ki-Shuk Shim ◽  
Gunyong An ◽  
Harald Höger ◽  
Gert Lubec

2012 ◽  
Vol 101 (3) ◽  
pp. 311-319 ◽  
Author(s):  
Ali Hosseini-Sharifabad ◽  
Mohammad Hossein Ghahremani ◽  
Omid Sabzevari ◽  
Naser Naghdi ◽  
Mohammad Abdollahi ◽  
...  

Endocrinology ◽  
2012 ◽  
Vol 153 (4) ◽  
pp. 1915-1924 ◽  
Author(s):  
Shan Wang ◽  
Xiaoyan Zhu ◽  
Binhai Cong ◽  
Xingji You ◽  
Yangkai Wang ◽  
...  

Urocortin (Ucn), a member of CRH family, has been implicated to be one of the endogenous regulators in the cardiovascular system and exerts its effects locally via an autocrine/paracrine fashion. Previous studies have shown the gender difference in CRH-induced vasodilation in human skin, which is related to the concentration of estrogens during the menstrual cycle. The aim of this study was to investigate whether estrogens modulate Ucn/CRH receptor type 2 (CRHR2) expression in vascular smooth muscle, thereby leading to vasodilation. We performed sham operation or bilateral ovariectomy (OVX) on female Sprague Dawley rats. OVX rats were sc administered 17β-estradiol (E2) at a dose of 30 μg/kg·d or with placebo for 12 wk. Primary smooth muscle cells of aorta were used for the in vitro study. It was found that the Ucn-induced vasodilation and CRHR2 expression were decreased in OVX rats and restored by E2 replacement treatment for 12 wk. E2 increased the expression of CRHR2 in cultured smooth muscle cells, which was blocked by estrogen receptor-β antagonist. Ucn significantly suppressed the phenylephrine-induced phospholipase Cβ3 activation, inositol 1,4,5-trisphosphate (IP3) production, and intracellular Ca2+ elevation. Ucn stimulated the expression of active GTP-bound Gαs protein and cAMP production. The suppressive effects of Ucn on phenylephrine-induced IP3 production and intracellular Ca2+ elevation were blocked by the inhibitors of adenylate cyclase and protein kinase A. Our results demonstrate that estrogen maintains the expression of CRHR2 in aorta smooth muscle, thereby enhancing vasodilator actions of Ucn. Ucn exerts its vasorelaxant effects via Gαs-cAMP-protein kinase A signaling, leading to down-regulation of the phospholipase Cβ-IP3-Ca2+ signaling pathway.


2004 ◽  
Vol 37 (1) ◽  
pp. 11-16 ◽  
Author(s):  
Dan-Ling Wang ◽  
Zhi-Qun Ling ◽  
Fu-Yuan Cao ◽  
Ling-Qiang Zhu ◽  
Jian-Zhi Wang

2008 ◽  
Vol 33 (9) ◽  
pp. 1811-1820 ◽  
Author(s):  
Xin-An Liu ◽  
Ling-Qiang Zhu ◽  
Qi Zhang ◽  
Hai-Rong Shi ◽  
Shao-Hui Wang ◽  
...  

2006 ◽  
Vol 26 (8) ◽  
pp. 2936-2946 ◽  
Author(s):  
Barbara Kaltschmidt ◽  
Delphine Ndiaye ◽  
Martin Korte ◽  
Stéphanie Pothion ◽  
Laurence Arbibe ◽  
...  

ABSTRACT Synaptic activity-dependent de novo gene transcription is crucial for long-lasting neuronal plasticity and long-term memory. In a forebrain neuronal conditional NF-κB-deficient mouse model, we demonstrate here that the transcription factor NF-κB regulates spatial memory formation, synaptic transmission, and plasticity. Gene profiling experiments and analysis of regulatory regions identified the α catalytic subunit of protein kinase A (PKA), an essential memory regulator, as a new NF-κB target gene. Consequently, NF-κB inhibition led to a decrease in forskolin-induced CREB phosphorylation. Collectively, these results disclose a novel hierarchical transcriptional network involving NF-κB, PKA, and CREB that leads to concerted nuclear transduction of synaptic signals in neurons, accounting for the critical function of NF-κB in learning and memory.


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