Experimental study of effect of corticosterone on primary cultured hippocampal neurons and their Ca2+/CaMK II expression

Sun Chenyou , Liu Nengbao , Li Honglian , Zhang Minhai , Liu Shaochun , Liu Xiangqian , Li Xiaoheng , Hong Xiaoping

Current Medical Science ›› 2004, Vol. 24 ›› Issue (6) : 543 -546.

PDF
Current Medical Science ›› 2004, Vol. 24 ›› Issue (6) : 543 -546. DOI: 10.1007/BF02911349
Article

Experimental study of effect of corticosterone on primary cultured hippocampal neurons and their Ca2+/CaMK II expression

Author information +
History +
PDF

Abstract

To explore the effect of different concentrations of corticosterone (CORT) on primary cultured hippocampal neurons and their Ca2+ CaMK II expression and possible mechanism, the changes of hippocampal neurons were observed in terms of morphology, activity of cells, cell death, concentrations of cytosolic free calcium, and the expression of CaMK II by using MTT assay, flow cytometry, fluorescent labeling of Fura-2/AM and Western blotting after 107. 10−6 and 106 mol/L of CORT was added to culture medium. The evident effect of 10−6 and 105 mol/L of CORT on the morphology of hippocampal neuron was found. Compared with control neurons, the activity of the cells was markedly decreased and [Ca2], increased in the neurons treated with 106 and 105 mol L of CORT, but no change was observed in the neuron treated with 106 mol/L of CORT. The death was either by way of apoptosis or necrosis in the cells treated with 106 and 105 mol/L of CORT respectively. The correlation analysis showed that a reverse correlation existed between [Ca2+], and the expression of CaMK II. Either apoptosis or necrosis occurs in the hippocampal neurons treated with CORT. The increased hippocampal [Ca2+], is both the results of CORT impairing the hippocampal neurons and the cause of the apoptosis of hippocampal neurons and the decreased CaMK II expression.

Keywords

corticosterone / hippocampal neurons / Ca2 / CaMKII

Cite this article

Download citation ▾
Sun Chenyou, Liu Nengbao, Li Honglian, Zhang Minhai, Liu Shaochun, Liu Xiangqian, Li Xiaoheng, Hong Xiaoping. Experimental study of effect of corticosterone on primary cultured hippocampal neurons and their Ca2+/CaMK II expression. Current Medical Science, 2004, 24(6): 543-546 DOI:10.1007/BF02911349

登录浏览全文

4963

注册一个新账户 忘记密码

References

[1]

McEwenB S, MagarinosS M. Stress effects on morphology and fuction of the hippocampus. Ann N Y Acad Sci, 1997, 721: 271-271

[2]

ChenH X, OtmakhovN, StrackS, et al. . Is persistent activity of calcium/calmodulin-dependent kinase required for the maintenance of LTP. J Neurophysio, 2001, 75: 1367-1367

[3]

TalmiM, CarlierE, Soumireu-MouratB. Similar effects of aging and coricosterone treatment on mouse hippocampus function. Neurobiol Aging, 1993, 14: 239-239

[4]

BrownR W, DiazR, RobsonA C, et al. . The ontogeny of 11β-hydroxysteroid dehydrogenate type 2 and mineral corticoid receptor gene expression reveal intricate control of glucocorticoid action in development. Endocrinology, 1996, 137(2): 794-794

[5]

ZhouJ Z, ZhengJ Q, ZhangY X, et al. . Corticosterone impairs cultured hippocampal neurons and facilitate Ca2+ influx through voltage-dependent Ca2− channel. Acta Pharmacol Sin, 2000, 21(2): 156-156

[6]

SapolskyR M, PackanD R, ValeW W. Glucocorticoid toxicity in the hippocampus:in vitro demonstration. Brain Res, 1988, 453(1–2): 367-367

[7]

VirginC E, HaT P, PachanD R, et al. . Glucocoricoids inhibit glucose transport and glutamate uptake in hippocompal astrocytes: implication for glucocoricoid. J Neurochem, 1991, 57: 1442-1442

[8]

PangZ, JamesW G. Mechanisms of cell death induced by the mitochondrial toxin 3-nitropropionic acid: acute excitotoxic necrosis and delayed apoptosis. J Neurosci, 1997, 17(9): 3061-3061

[9]

ZhouJ Z, ZhangY X, ZhouJ H. Increased levels of corticosterone in plasma and hippocampus and their relationship with hippocampal ATP deleption in senescence-accelerated mouse P8. Chin J Pharmacol Toxicol, 1998, 12: 12-12

[10]

JohnstonD, WilliamsS, JaffeD, et al. . NMDA-receptor-independent long-term potentiation. Ann Rev Phsiol, 1992, 54: 489-489

[11]

MichaelJ B, MartinD B, PeterL. Calcium-a life and death signal. Science, 1998, 395: 645-645

[12]

ShenK, MeyerT. Dynamic control of CaMKII translocation and localization in hippocampal neurons by NMDA receptor stimulation. Science, 1999, 284: 162-162

[13]

BesharseJ C. Coupling and activated MAP kinas to circadian clock output. Neuron, 2001, 29(1): 3-3

[14]

McgaughJ L. Memory-a century of a consolidation. Science, 2000, 287(5451): 248-248

[15]

KobayashiH, FukudaH. Involvement of calmodulin and calmodulin-binding proteins int the differentiation of treachery elements in Zinnia mesophyll cells. Protoplasma, 1994, 138: 69-69

AI Summary AI Mindmap
PDF

104

Accesses

0

Citation

Detail

Sections
Recommended

AI思维导图

/