柴真
脑损伤和修复过程中神经元钙稳态的调控机制。神经元和胶质细胞低氧损伤或适应的细胞机制。 细胞因子及其信号转导途径在体温调节中的作用。
个性化签名
- 姓名:柴真
- 目前身份:
- 担任导师情况:
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学术头衔:
博士生导师
- 职称:-
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学科领域:
神经生物学
- 研究兴趣:脑损伤和修复过程中神经元钙稳态的调控机制。神经元和胶质细胞低氧损伤或适应的细胞机制。 细胞因子及其信号转导途径在体温调节中的作用。
工作经历:
2007 - now , 教授 , 北京大学生命科学学院
1997 - 2007 , 副教授 , 北京大学生命科学学院
1988 - 1993 , 讲师 , 北京大学生命科学学院
教育经历:
1993 - 1997 , 理学博士 , 神经化学和神经毒理学 , 瑞典斯德哥尔摩大学 (Stockholm University, Sweden),
1979 - 1983 , 理学学士 , 生理学 , 北京大学
荣誉:
北京市教育教学成果一等奖 , 2008
国家级教学成果一等奖 , 2005
北京市教育教学成果一等奖 , 2004
科研领域:
脑损伤和修复过程中神经元钙稳态的调控机制。
神经元和胶质细胞低氧损伤或适应的细胞机制。
细胞因子及其信号转导途径在体温调节中的作用。
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443
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成果数
8
【期刊论文】Dark rearing alters the short-term synaptic plasticity in visual cortex
柴真, Ai-Hui Tang, Zhen Chai, Shi-Qiang Wang ∗
Neuroscience Letters 422(2007)49-53,-0001,():
-1年11月30日
The strength of all chemical synapses can be rapidly up- or down-regulated by their recent activities to reshape the postsynaptic signal through a mechanism of short-term facilitation or depression. It is also true that sensory experience is essential for maturation of cortical circuits and function. We studied the effect of sensory experience on the short-term plasticity in brain slices of rat visual cortex. Repetitive stimulation was applied in layer II/III and the response of pyramidal neuron in layer V was examined by whole-cell recording. We deprived the visual experience of rats by rearing the animals in dark environment.We found that dark rearing (DR) had no effects on paired-pulse interactions of either excitatory postsynaptic currents (EPSCs) or inhibitory postsynaptic currents (IPSCs). However, DR increased the level of IPSCs steady-state depression at stimulation frequency of 20 Hz or more. This result, together with the finding that DR reduced the excitability of neural circuit in visual cortex, suggested a compensatory mechanism, which may be important in enhancing the network excitability at a time when synapses are immature.
Short-term depression, Dark-rear, Visual cortex, Experience, Steady-state depression, Paired-pulse depression, Excitation/, inhibition balance
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【期刊论文】Full-length article Cellular mechanism for spontaneous calcium oscillations in astrocytes1
柴真, Tong-feiWANG, Chen ZHOU, Ai-hui TANG, Shi-qiangWANG, Zhen CHAI
Acta Pharmacologica Sinica 2006 Jul; 27(7): 861-868,-0001,():
-1年11月30日
Aim: To determine the Ca2+ source and cellular mechanisms of spontaneous Ca2+ oscillations in hippocampal astrocytes. Methods: The cultured cells were loaded with Fluo-4 AM, the indicator of intracellular Ca2+, and the dynamic Ca2+ transients were visualized with confocal laser-scanning microscopy. Results: The spontaneous Ca2+ oscillations in astocytes were observed first in co-cultured hippocampal neurons and astrocytes. These oscillations were not affected by tetrodotoxin (TTX) treatment and kept up in purity cultured astrocytes. The spontaneous Ca2+ oscillations were not impacted after blocking the voltage-gated Ca2+ channels or ethylenediamine tetraacetic acid (EDTA) bathing, indicating that intracellular Ca2+ elevation was not the result of extracellular Ca2+ influx. Furthermore, the correlation between the spontaneous Ca2+ oscillations and the Ca2+ store in endoplasmic reticulum (ER) were investigated with pharmacological experiments. The oscillations were: 1) enhanced when cells were exposed to both low Na+ (70mmol/L) and high Ca2+ (5mmol/L) solution, and eliminated completely by 2 μmol/L thapsigargin, a blocker of sarcoplasmic reticulum Ca2+-ATPase; and 2) still robust after the application with either 50 μmol/L ryanodine or 400 μmol/L tetracaine, two specific antagonists of ryanodine receptors, but depressed in a dose-dependent manner by 2-APB, an InsP3 receptors (InsP3R) blocker. Conclusion: InsP3R-induced ER Ca2+ release is an important cellular mechanism for the initiation of spontaneous Ca2+ oscillation in hippocampal astrocytes.
hippocampal astrocytes, spontaneous Ca2+, oscillations, endoplasmic reticulum Ca2+, store, InsP3 receptors, confocal laser scanning microscope
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【期刊论文】Temperature Dependence and Thermodynamic Properties of Ca21 Sparks in Rat Cardiomyocytes
柴真, Yu Fu, Guang-Qin Zhang, Xue-Mei Hao, Cai-Hong Wu, Zhen Chai, and Shi-Qiang Wang
Biophysical Journal Volume 89 October 2005 2533-2541,-0001,():
-1年11月30日
To elucidate the temperature dependence and underlying thermodynamic determinants of the elementary Ca21 release from the sarcoplasmic reticulum, we characterized Ca21 sparks originating from ryanodine receptors (RyRs) in rat cardiomyocytes over a wide range of temperature. From 35 C to 10 C, the normalized fluo-3 fluorescence of Ca21 sparks decreased monotonically, but the D[Ca21]i were relatively unchanged due to increased resting [Ca21]i. The time-to-peak of Ca21 sparks, which represents the RyR Ca21 release duration, was prolonged by 37% from 35 C to 10 C. An Arrhenius plot of the data identified a jump of apparent activation energy from 5.2 to 14.6 kJ/mol at 24.8 C, which presumably reflects a transition of sarcoplasmic reticulum lipids. Thermodynamic analysis of the decay kinetics showed that active transport plays little role in early recovery but a significant role in late recovery of local Ca21 concentration. These results provided a basis for quantitative interpretation of intracellular Ca21 signaling under various thermal conditions. The relative temperature insensitivity above the transitional 25 C led to the notion that Ca21 sparks measured at a "warm room" temperature are basically acceptable in elucidating mammalian heart function.
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柴真, KATARINA ALHEIM*, ZHEN CHAI*, GIAMILA FANTUZZI†, HOMA HASANVAN*, DAVID MALINOWSKY*, ELENA DI SANTO‡, PIETRO GHEZZI‡, CHARLES A. DINARELLO†, AND TAMAS BARTFAI*§
Proc. Natl. Acad. Sci. USA Vol.94, pp. 2681-2686, March 1997,-0001,():
-1年11月30日
IL-β is an endogenous pyrogen that is inducedduring systemic lipopolysaccharide (LPS)- or IL-1-induced fever. We have examined the fever and cytokineresponses following i.p. injection of IL-1 agonists, IL-1a andIL-β, and compared these with response to LPS (i.p.) in wild-type and IL-β-deficient mice. The IL-β deficient mice appear to have elevated body temperature but exhibit a normal circadian temperature cycle. Exogenously injected IL-β, IL-1a, or LPS induced hyperresponsive fevers in the IL-βdeficient mice. We also observed phenotypic differences between wild-type and IL-β-deficient mice in hypothalamic basal mRNA levels for IL-1a and IL-6, but not for IL-βconverting enzyme or IL-1 receptor type I or type II. The IL-1a mRNA levels were down-regulated, whereas the IL-6 mRNA levels were up-regulated in the hypothalamus of IL-βdeficient mice as compared with wild-type mice. The IL-βdeficient mice also responded to LPS challenge with significantly higher serum corticosterone and with lower serum tumor necrosis factor type a levels than the wild-type mice. The data suggest that, in the redundant cascade of proinflammatory cytokines, IL-β plays an important but not obligatory role in fever induction by LPS or IL-1a, as well as in the induction of serum tumor necrosis factor type a and corticosterone responses either by LPS or by IL-1a or IL-β.
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柴真, By Z. Chai, * S. Gatti, * C. Toniatti, * V. Poli, * and T. Bartfai*
Brief Definitive Report, Published January 1, 1996, Volume 183, January 1996 311-316,-0001,():
-1年11月30日
Interleukin (IL)-β, IL-β, and tumor necrosis factor 0r (TNF-ot) are considered to act as endogenous pyrogens. Because of the complex pattern of cross-inductions between these cytokines, the relative role of the central and peripheral production of these cytokines in eliciting the fever response has not yet been clarified. The purpose of this study was to determine the role of IL-Β in the fever response by making use of mice carrying a null mutation in the IL-β gene. The intraperitoneal injections oflipopolysaccharide (LPS) (50bLg/kg) and recombinant murine (rm) IL-β (10 bg/kg), respectively, failed to evoke fever response in IL-β-deficient mice, whereas the same doses of LPS and rmIL-βcaused fever response in wild-type mice. The fever response could be induced in the IL-β-deficient mice by intracerebroventricular injection of recombinant human (rh) IL-β (500 ng/mouse), whereas intracerebroventricular injection of rmlL-β (100 ng/mouse) failed to produce fever response in the IL-β-deficient mice. These results suggest that central IL-Β is a necessary component of the fever response to both endogenous (IL-β) and exogenous (LPS) pyrogens in mice and that IL-β acts downstream from both peripheral and central IL-β.
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柴真, Johan Lundkvista, Zhen Chaia, , Roya Teheraniana, Homa Hasanvana, Tamas Bartfaia, *, Francois Jenck b, Ulrich Widmer b, Jean-Luc Moreaub
European Journal of Pharmacology 309(1996)195-200,-0001,():
-1年11月30日
The multiple actions of corticotropin-releasing factor (CRF) on neuroendocrine and behavioural functions can now be examined using new, high affinity, non peptidic antagonists which exhibit central activity upon systemic application. We have shown that compound CP 154,526 (butyl-ethyl-[2.5-dimethyl-7-(2、4、6-trimethyphenyl)-7H-pyrrtly [2.3d]pyrimidin-4-yl]amine) displaces [125][Tyo]CRF from rat hippocampal CRF receptors (ICso= 0.5 nM) and from pituitary CRF receptors (ICso=0.04 nM). The same compound inhibits in a concentration-dependent manner the ovine CRF (0.1 ixM)-stimulated adenylate cyclase activity in membranes of a mouse pituitary adenoma cell line, AtT20, with an ICso value of 50 nM. Systemic application of the CRF receptor antagonist (0.16mg/kgi.p.) blocked recombinant human interleukin-ll3 (5p.g/kgi.p.) induced fever in rats. The CRF receptor antagonist CP 154,526 (lmg/kgi.p.) also exhibited signs of anxiolytic-like activity in the elevated plus-maze test in rats.
CRF (, corticotropin-releasing factor), , Anxiety, Interleukin-l3, Fever, CRF receptor antagonist
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柴真, Z. Chai, K. Alheim, J. Lundkvist, S. Gatti, T. Bartfai
CYTOKINE, Vol.8, No.3 (March), 1996: pp 227-237,-0001,():
-1年11月30日
Subchronic (36 h) exposure of rats to corticosterone (CS) (100 mg/pellet, subcutaneously), blocked the pyrogenic response to recombinant human interleukin 1b (rhIL-1b, 5 mg/kg, ip.). CS treatment reduced the basal mRNA levels of IL-1a and IL-1b, but elevated the mRNA levels of IL-6 in the hypothalamus and hippocampus as shown by RT-PCR. The CS treatment clamped the cytokine mRNA levels, and injection of rhIL-1b to CS treated rats did not significantly affect these altered mRNA levels. IL-6 bioactivity in serum was not significantly changed by CS treatment, but increased 50 times upon injection of rhIL-1b. rhIL-1b caused a significantly lower induction of serum IL-6 levels in CS pretreated rats (9-fold). The pyrogenic response to injection of rhIL-1b has returned 5 days after the removal of the corticosterone pellet, and the hypothalamic cytokine mRNA levels (IL-1a, IL-1b and IL-6) have returned to basal. These results suggest that altered and clamped hypothalamic IL-1a, IL-1b and IL-6 mRNA levels may be involved in the antipyretic effects of a pretreatment with high doses of CS and that these CS effects are rapidly reversible.
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柴真, David Malinowskya, Zhen Chaia, Jesper Bristulfa, Andras Simoncsitsb, Tamas Bartfa&*
Neuroscience Letters 201 (1995) 33-36,-0001,():
-1年11月30日
The interleukin-1 (IL-l) system possesses two distinct receptors (type I and type II) which, together with the accessory protein, mediate a multitude of responses to IL-la and IL-l@, including fever. So far, no receptor subtype-specific ligands have been described. Since both types of IL-l receptors occur in the thermoregulatory areas it was unclear which IL-l receptor type mediates fever. We report here that for a series of deletion mutants of human recombinant IL-lb (hrIL-l/I), the affinity of these ligands for the type I IL-1 receptor correlates with their efficacy to evoke the fever response (hrIL-l/I>des-SND 52-54>des-QGE48-50>des-156). Thus, the results suggest that agonist occupancy of the type I IL-l receptor is essential for IL-l/I-mediated fever.
Interleukin-1, Fever, Endogenous pyrogen, Hypothalamus, Receptors, Mutagenesis, Deletion
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