Protective mechanism of fetal brain against hypoxia: in vivo optical recordings
胎儿脑缺氧的保护机制:体内光学记录
基本信息
- 批准号:13671138
- 负责人:
- 金额:$ 2.3万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:2001
- 资助国家:日本
- 起止时间:2001 至 2002
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
It is known that fetal brain is strong against hypoxia. During delivery, intermittent severe hypoxia on fetus lasts for a long time. However, Almost fetus was born without the brain damage. Therefore, it is thought the fetal brain may have protective mechanism against hypoxia. We studied the protective mechanism by forcusing on glutaminergic synaptic transmission, using the optic imaging system. The termed pregnant rat (Sprague Dawly rat, 3 months old) was anesthetized with uretane (1.2-1.4 g/kg, i. P.). The fetus which was connected with dam by umbilical cord, was fixed on a stereotaxic instrument. The uterus was exposed by caesarean section and partially cut to exposure of the fetus. For electrical stimulation of the fetal superior colliculus (SC), a bipolar electrode (stainless steel wire) was inserted into the rostral part of the SC. Focal stimulation of the SC was made by a single pulse or train pulse (10 pulses) at currents of 1-3 mA. Fluorescent Ca2+ sensitive dye (Fura-2/AM ) w … More as loaded into the SC regions for 90 min. The fractional changes in fluorescence of Ca2+ sensitive dye were recorded by an optical imaging system (ARGUS/HiSCA). The fetus with the dam was set under the microscope. The acute hypoxia was performed with occluding the umbilical cord by a fine clip.1) [Ca2+]I in SC was increased during with the occlusion of the umbilical cord and recovered gradually after the release of the umbilical cord occlusion. The increased [Ca2+]I was attenuated by NMDA receptor antagonist (AP-5) after pretreatment with non-NMDA receptor antagonist (CNQX ).2) [Ca2+]I in the SC regions was steeply increased by the focal SC stimulation of the train pulses (the early response). Increasing the stimulus current from 1 to 3 mA produced greater increases in [Ca2+]i. The train pulse stimulation induced a prolonged response (>10 sec) (the late response). The early response was antagonized with CNQX and AP-5. The late response was antagonized by AP-5.3) At 3hrs after the occlusion of umbilical cord, the early response was induced with the focal SC stimulation, but the late response was markedly reduced. The early response was antagonized by CNQX but not almost by AP-5.These results suggest that the Ca2+influx following focal SC stimulation and hypoxia in fetal rats is mediated by glutaminergic synapse transmission. Further, after receiving hypoxia, NMDA receptor may be inactivated with a lapse of time. This may contribute to protect fetal brain from an excess of Ca2+influx. Less
众所周知,胎儿大脑对缺氧有很强的抵抗力。分娩过程中,胎儿间歇性严重缺氧持续时间长。然而,几乎胎儿出生时没有脑损伤。因此,人们认为胎儿大脑可能具有抗缺氧的保护机制。本实验采用光学成像系统,通过对多巴胺能神经元突触传递的影响,研究了其保护机制。孕鼠(SpragueDawly大鼠,3月龄)用乌拉坦(1.2- 1.4g/kg,i. P.)。将胎儿与母体通过脐带连接,固定在立体定位仪上。通过剖腹产暴露子宫,并部分切割以暴露胎儿。电刺激胎儿上级丘(SC)时,将双极电极(不锈钢丝)插入SC的喙部,以1-3 mA的电流,用单脉冲或串脉冲(10个脉冲)进行SC的局灶性刺激。荧光钙敏感染料(Fura-2/AM)w ...更多信息 通过光学成像系统(ARGUS/HiSCA)记录Ca 2+敏感染料荧光的分数变化。带着母体的胎儿被放在显微镜下。1)脐带阻断过程中SC内[Ca ~(2+)]I升高,脐带阻断解除后逐渐恢复。用非NMDA受体拮抗剂(CNQX)预处理后,NMDA受体拮抗剂(AP-5)可抑制SC区[Ca ~(2+)] i的增加。刺激电流从1 mA增加到3 mA,[Ca 2 +]i增加幅度更大。串脉冲刺激诱导延长的反应(>10秒)(迟发反应)。早期反应被CNQX和AP-5拮抗。AP-5可拮抗迟发反应。3)阻断脐带后3 h,刺激SC可诱发早期反应,但迟发反应明显减弱。CNQX能拮抗早期反应,AP-5几乎不能拮抗早期反应。提示局灶性SC刺激和缺氧引起的胎鼠Ca ~(2+)内流是由多巴胺能突触传递介导的。此外,在接受缺氧后,NMDA受体可能随着时间的推移而失活。这可能有助于保护胎脑免受过量的Ca 2+内流。少
项目成果
期刊论文数量(17)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Sakata, Y.: "Paradoxical rise in brainstem PO2 following umbilical cord occlusion in full-term rat fetuses"Neuroscience Letters. 330. 167-170 (2002)
Sakata, Y.:“足月大鼠胎儿脐带闭塞后脑干 PO2 出现矛盾上升”《神经科学快报》。
- DOI:
- 发表时间:
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- 影响因子:0
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- 通讯作者:
Fujioka, T.: "Materno-fetal coordination of stress-induced Fos expression in the hypothalamic praventricular nucleus during pregnancy"Neuroscience. (in press). (2003)
Fujioka, T.:“怀孕期间下丘脑室前核中应激诱导的 Fos 表达的母胎协调”神经科学。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
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- 通讯作者:
Y. Sakata: "Paradoxical rise in brainstem PO2 following unbilical cord occlusion in full-term rat fetuses"Neurosci. Lett.. 330. 167-170 (2002)
Y. Sakata:“足月大鼠胎儿脐带闭塞后脑干 PO2 出现矛盾上升”Neurosci。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
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- 通讯作者:
坂田義行: "In vivo胎仔脳における光学的イメージング法の適用"山口医学. 50・4. 693-696 (2001)
Yoshiyuki Sakata:“光学成像方法在体内胎儿大脑中的应用”山口医学50・4。
- DOI:
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- 影响因子:0
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- 通讯作者:
Jqbal Chowdhury, G.M.: "Cortical spreading depression affects Fos expression in the hypothaLamic paraventricular nucleus and the cerebral cortex of both hemispheres"Neuroscience Research. (in press). (2003)
Jqbal Chowdhury, G.M.:“皮质扩散抑制影响下丘脑室旁核和两个半球大脑皮层的 Fos 表达”神经科学研究。
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- 影响因子:0
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SAKATA Yoshiyuki其他文献
SAKATA Yoshiyuki的其他文献
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{{ truncateString('SAKATA Yoshiyuki', 18)}}的其他基金
Protection mechanism of fetal brain against severe hypxia : analysis of micro RNA using with in vivo optical imaging
胎儿大脑对严重缺氧的保护机制:利用体内光学成像分析微小RNA
- 批准号:
19591279 - 财政年份:2007
- 资助金额:
$ 2.3万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
The role of Bcl-2 and Bax in hypoxia-induced caspase-3 activation in the fetal superior colliculus: in vivo optical
Bcl-2 和 Bax 在缺氧诱导胎儿上丘 caspase-3 激活中的作用:体内光学
- 批准号:
17591143 - 财政年份:2005
- 资助金额:
$ 2.3万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Effects of hypoxia on caspase-3 activity in fetal superior colliculus : in vivo optical imagings
缺氧对胎儿上丘 caspase-3 活性的影响:体内光学成像
- 批准号:
15591157 - 财政年份:2003
- 资助金额:
$ 2.3万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Physiological role of cytokines on homeostasis
细胞因子对体内平衡的生理作用
- 批准号:
03404018 - 财政年份:1991
- 资助金额:
$ 2.3万 - 项目类别:
Grant-in-Aid for General Scientific Research (A)
Production of antiserum against pyrogenic factor and pyrogenic mechanisms using the antiserum.
抗致热因子抗血清的生产以及使用该抗血清的致热机制。
- 批准号:
61570086 - 财政年份:1986
- 资助金额:
$ 2.3万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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