Archive

26 February 2012, Volume 2 Issue 1 Previous Issue    Next Issue

---

For Selected:

Download Citations EndNote Ris BibTeX

Toggle Thumbnails

Select

Total Saponins from Rhizoma Anemarrhenae Increase Acetylcholinesterase Activity in the Hippocampus of Diabetic Rats ZHAI Yun-peng, ZHU Xia, LU Qian, WANG Jian-yun, YIN Xiao-xing, LIU Yao-wu 2012, 2 (1):  1-9.  Abstract ( 3983 )   PDF (1075KB) ( 2616 )   Objective: To investigate the effects of total saponins from Rhizoma Anemarrhenae (TS) on acetylcholinesterase (AchE) activity in the hippocampus of streptozotocin-induced diabetic rats and their possible mechanisms. Methods: Diabetic rats were treated with TS (200 mg?kg-1, ig.) for 8 weeks, and their blood glucose and body weight were measured monthly and weekly, respectively. The hippocampus was obtained for assays of AchE activity as well as levels of malondialdehyde (MDA) and reduced glutathione (GSH); blood was collected for assays of levels of MDA, GSH and glucose. Results: Compared with that of the age-matched normal rats, AchE activity was markedly increased in the hippocampus of diabetic rats, and TS treatment blocked such an increase. Meanwhile, diabetes significantly elevated the MDA level and reduced GSH level both in the hippocampus and the serum, and TS treatment significantly prevented such changes. In addition, TS significantly decreased the fasting blood glucose level and increased the body weights of diabetic rats. Conclusion: TShas an inhibitory effect on AchE activity in the hippocampus in diabetic rats, which is at least partly due to its antioxidant and anti-diabetic activity. References | Related Articles | Metrics

Select

Involvement of Large-conductance Ca2+-activated K+ Channels in the Synaptic Transmission in the Lateral Amygdala GUO Yan-yan, QI Feng-yan, ZHAO Ming-gao 2012, 2 (1):  10-19.  Abstract ( 3507 )   PDF (7908KB) ( 1388 )   Objective: Large-conductance Ca2+-activated K+ (BKCa) channels are highly expressed in the lateral amygdala (LA), which is involved in stress disorders, but the role of these BKCa in the neuronal circuits are poorly understood. In the previous study, we found a significant reduction in BKCa channel expression in the amygdala of mice undergoing acute stress, which was accompanied by anxiety-like behaviors. In this study, we focused on the role of BKCa channels in the synaptic transmission and plasticity in the lateral amygdala. Methods: Behavioral tests, western-blot analysis and electrophysiological recordings were performed. Results: First, we found the co-distribution of BKCa channels immunoreactively with glutamatergic neuronal marker CaMKIIα or interneuron marker GAD-65 in the LA. In addition, both NR2A and NR2B were co-localized with the BKCa channels and formed a heteroreceptor complex in the soma and dendrites of the amygdala neurons. Furthermore, block of the BKCa channels notably facilitated long-term potentiation (LTP) induction at the thalamo-LA synapse. Conclusion: BKCa channels play critical roles in the synaptic plasticity in the LA. References | Related Articles | Metrics

Select

Involvement of Water Channel Aquaporin 4 in the Nervous Disorders WANG Wei-ling，YANG Bao-xue 2012, 2 (1):  20-27.  Abstract ( 4212 )   PDF (3828KB) ( 3255 )   The aquaporins (AQP) are a family of water-transporting proteins. Aquaporin4 (AQP4) is expressed in astrocytes throughout the central nervous system, as well as in Müller cells in the retina, Claudius/Hensen cells in the inner ear and olfactory epithelial cells. There are two AQP4 isoforms, M1 and M23， produced by alternative splicing. M23 AQP4 forms heterotetramers that assemble in the cell membrane in supramolecular structures called orthogonal arrays of particles (OAP). Phenotype analysis of AQP4-null mice indicates the involvement of AQP4 in brain and spinal cord water balance, astrocyte migration, neural signal transduction and neuroinflammation. AQP4-null mice manifest reduced brain swelling in cytotoxic cerebral edema, but increased brain swelling in vasogenic edema and hydrocephalus. AQP4 deficiency increases seizure duration. AQP4 is also involved in the neuroin?ammatory demyelinating disease neuromyelitis optica, where autoantibodies (NMO-IgG) targeting AQP4 produce astrocyte damage and in?ammation. This review summarizes the effect and possible mechanism of AQP4 in nervous system diseases, such as epilepsy, edema and neuromyelitis optica. References | Related Articles | Metrics

Select

The Neuroprotective Effect of Estrogen is Associated with Regulation Energy Metabolism SHEN Li-xia, ZHANG Dan-shen 2012, 2 (1):  28-32.  Abstract ( 3306 )   PDF (797KB) ( 2207 )   Estrogen has been demonstrated to be involved in the development and progress of Alzheimer's disease. Numerous studies show the neuroprotective effects of estrogen, but the underlying mechanism remains unclear. Here, we discussed the neuroprotective effects of estrogen, particularly focusing on the energy metabolism related to improvement of glucose metabolism, regulation of the brain metabolism and enhancement of mitochondrial function. Application of estrogen or estrogen substitutes to maintain the nervous system function and to prevent and control Alzheimer's disease could be a fruitful field in future studies. References | Related Articles | Metrics

Select

Endoplasmic Reticulum Stress and Metabolic Syndrome: Mechanisms and Therapeutic Potential XIA Zhi, ZHANG Ying-mei, REN Jun 2012, 2 (1):  33-44.  Abstract ( 3742 )   PDF (964KB) ( 2750 )   The nomenclature "metabolic syndrome" refers to a cluster of disorders including obesity, dyslipidemia, hypertension, and insulin resistance. It is a primary risk factor for cardiovascular and neurological diseases accompanied by dysregulated adipokines (cytokines and chemokines) and leptin, a peptide hormone secreted by white adipose tissue. These changes modulate immune and inflammatory responses, prompting the reset of the hypothalamic “body weight/appetite/satiety set point”. The precise tie between metabolic syndrome and neurological disorders such as stroke, depression and Alzheimer's disease remains largely elusive. A number of cellular and molecular mechanisms have been put forward for the metabolic syndrome-associated cardiovascular and neurological anomalies including oxidative stress, alteration in glucose and lipid metabolism, abnormal insulin and leptin signaling, apoptosis, and autophagy. More recent evidence depicted that endoplasmic reticulum (ER) stress, also known as unfolded protein response (UPR), gets activated in the context of metabolic syndrome. Hypothalamic ER stress leads to inflammation and resistance to leptin/insulin signaling. Hepatic ER stress promotes the onset and development of insulin resistance while ER stress in adipose tissues facilitates inflammation to cause secretion of adipokines. To the contrary, inflammation aggravates ER stress. ER stress activates autophagy while autophagy induction may, in turn, enhance ER stress. These interplays between ER stress and cell injurious machinery compromise insulin signaling, thereby contributing to the onset and development of metabolic syndrome. This synthetic min-review of recent literature not only describes the involvement of cardiovascular and neurological systems in the pathogenesis of metabolic syndrome, but also dissects the role of ER stress as well as its interplay with autophagy and inflammation in cardiovascular and neurological disorders in metabolic syndrome. References | Related Articles | Metrics

Select

In Vivo Application of Two-photon Microscopy in Neuropharmacological Research ZHAO Jun,WANG Jin-hui 2012, 2 (1):  45-64.  Abstract ( 5127 )   PDF (6504KB) ( 5908 )   Two-photon microscope is an useful and advanced tool for noninvasive deep fluorescence imaging in the intact brain tissue of living animals. Due to nonlinear two-photon effects, two-photon microscope enables long-term imaging in vivo with deeper detection, higher signal-to-noise ratio and lower photodamage, compared to wide-field and confocal microscopy. Two-photon microscopy can provide high-resolution images to study cellular and subcellular structure and function, including morphology, mobility and intracellular ions of cells. On the other hand, large scale two-photon imaging of cell population reveals the network construction and activity dynamics with single-cell resolution, which makes two-photon microscopy a high throughput tool in system pharmacology. Moreover, two-photon microscopy can offer some precise optical operations, such as photolysis, photoactivation, phototransfection and photodamage. Here, we give an introduction to the principles of two-photon microscopy and its in vivo applications in neuroscience and neuropharmacology researches. References | Related Articles | Metrics