984 resultados para Xiong, Culü, 1635-1709,
Resumo:
It has been documented that stress or glucocorticoids have conflicting effects on memory under different conditions. However, it is not fully understood why stress can either impair or enhance memory. Here, we have examined the performance of six age groups of Wistar rats in a water maze spatial task to evaluate the effects of stress under different conditions. We found that the impairment or enhancement effect of an 'elevated platform' (EP) stress on memory was dependent on previous stress experience and on age. EP stress impaired memory retrieval in water maze naive animals. but enhanced rather than impaired memory retrieval in young water maze stress-experienced animals. Furthermore, exogenously applied corticosterone or foot shock stress before water maze training prevented the impairment of memory retrieval that should be induced by treatment with corticosterone or foot shock before the 'probe trial'. Again, memory retrieval was enhanced in young animals under these conditions, and this enhancement can be prevented by the glucocorticoid receptor antagonist RU 38486. Thus, glucocorticoid receptor activation not only induced impairment of memory but also increased the capacity of young animals to overcome a later stress. The present findings suggest that the effect of stress on memory can be switched from impairment to enhancement dependent on both stress experience and age.
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Memory is sensitive to the short-acting anesthetic (2,6-diisopropylphenol) propofol, but the underlying mechanism is little known. Here, we have examined the effects of propofol on synaptic plasticity in the CA1 region of the hippocampus of anesthetized rats. We found that low dose of propofol (20 mg/kg, i.p.) did not affect the basal transmission, but enhanced prominently the development of long-term depression (LTD) and impaired the maintenance of long-term potentiation (LTP). The impairment of LTP maintenance and enhancement of LTD development may contribute to propofol-induced deficits in memory following propofol anesthesia. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
Resumo:
Behavioral stress can either block or facilitate memory and affect the induction of long-term potentiation (LTP) and long-term depression (LTD). However, the relevance of the stress experience-dependent long-term depression (SLTD) to spatial memory task is unknown. Here we have investigated the effects of acute and sub-acute elevated platform (EP) and foot shock (FS) stress on LTD induction in CA1 region of the hippocampus of anesthetized rats and spatial memory in Morris water maze. We found that LTD was facilitated by acute EP stress, but not by sub-acute EP stress that may be due to the fast adaptation of the animals to this naturalistic mild stress. However, FS stress, an inadaptable strong stress, facilitated LTD induction both in acute and sub-acute treatment. In addition, with the same stress protocols, acute EP stress impaired spatial memory but the sub-acute EP stressed animals performed the spatial memory task as well as the controls, may due to the same reason of adaptation. However, acute FS stress slightly impaired learning but sub-acute FS even enhanced memory retrieval. Our results showed that SLTD was disassociated with the effect of stress on memory task but might be related to stress experience-dependent form of aberrant memory. (C) 2003 Elsevier Science Ireland Ltd. and the Japan Neuroscience Society. All rights reserved.
Resumo:
Not all experiences are memorized equally well. Especially, some types of stress are unavoidable in daily life and the stress experience can be memorized for life. Previous evidence has showed that synaptic plasticity, such as long-term potentiation (LTP) that may be the major cellular model of the mechanism underlying learning and memory, is influenced by behavioral stress. However, the effect of behavioral stress on age-related synaptic plasticity in-vivo was primarily known. Here we found that the LTP induction in the hippocampal CA1 region of anesthetized rats obviously showed inverted-U shape related to ages (4, 10 and 74 weeks old rats), but low-frequency stimulation was unable to induce reliable long-term depression (LTD) in these animals. Furthermore, acute elevated platform (EP) stress enabled reliable LTD significantly and completely blocked LTP induction at these ages. Importantly, LTD after exposure to acute EP stress showed similar magnitude over these ages. The present results that stress enables LTD but impairs LTP induction at these three ages strengthen a view that stress experience-dependent LTD (SLTD) may underlie stress form of aberrant memories. (C) 2004 Elsevier B.V. All rights reserved.
Resumo:
The subiculum, which is the primary target of CA1 pyramidal neurons and sending efferent fibres to many brain regions, serves as a hippocampal interface in the neural information processes between hippocampal formation and neocortex. Long-term depression (LTD) is extensively studied in the hippocampus, but not at the CA1-subicular synaptic transmission. Using whole-cell EPSC recordings in the brain slices of young rats, we demonstrated that the pairing protocols of low frequency stimulation (LFS) at 3 Hz and postsynaptic depolarization of -50 mVelicited a reliable LTD in the subiculum. The LTD did not cause the changes of the paired-pulse ratio of EPSC. Furthermore, it did not depend on either NMDA receptors or voltage-gated calcium channels (VGCCs). Bath application of the G-protein coupled muscarinic acetylcholine receptors (mAChRs) antagonists, atropine or scopolamine, blocked the LTD, suggesting that mAChRs are involved in the LTD. It was also completely blocked by either the Ca2+ chelator BAPTA or the G-protein inhibitor GDP-beta-S in the intracellular solution. This type of LTD in the subiculum may play a particular role in the neural information processing between the hippocampus and neocortex. (c) 2005 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.
Resumo:
Previous Studies have demonstrated that in the pentylenetetrazol (PTZ) kindling model, recurrent seizures either impair or have no effect on learning and memory. However, the effects of brief seizures on learning and memory remain unknown. Here, we found
Resumo:
为了比较不同地域萤火虫荧光素酶基因的进化关系,通过GenBank中已知的荧光素酶基因保守区段设计引物,利用5'-RACE(rapid-amplification of cDNA ends)和3'-RACE技术克隆了来自云南省文山州和西双版纳州的同种卵黄萤荧光素酶基因cDNA和全基因序列.来自不同地域的2种卵黄萤荧光素酶在基因序列上存在3个不同碱基位点,但是它们编码的荧光素酶只存在1个不同的氨基酸.卵黄萤荧光素酶基因全长(从起始密码子到终止密码子)1998 bp,包含7个外显子,6个内含子,其cDNA序列共1976 bp,包含102 bp 5'UTR(untranslated region)、1635 bp的荧光素酶基因开放阅读框和239 bp的3'UTR序列.卵黄萤荧光素酶基因的开放阅读框编码1个544个氨基酸的蛋白质,比同属的其它几种荧光素酶少4个氨基酸.来自2个不同地域的卵黄萤荧光素酶在进化上是比较保守的,它们与北美萤火虫Photinus pyralis荧光素酶在碱基序列上分别有62.9%和63%相似性.
Resumo:
按照Promega 公司的mRNA 提取试剂盒操作手册, 从圆斑蝰蛇( Daboia russellii siamensis ) 的毒腺中提 取mRNA ; 利用RT2PCR 的方法进行体外扩增, 获得C - 型凝集素蛋白的基因, 克隆到pMD182T 载体中。随机挑 选14 个阳性克隆进行核酸测序, 获得7 个编码不同蛇毒C - 型凝集素样蛋白亚基的cDNA , 分别命名为DRS2L1 、 DRS2L2 、DRS2L3 、DRS2L4 、DRS2L5 、DRS2L6 和DRS2L7 。由基因序列推导出的氨基酸序列表明, 克隆到的7 个蛇 毒C - 型凝集素样蛋白的亚基中均有糖识别结构域存在。BLAST 分析显示, 仅有DRS2L1 的蛋白序列与目前已知 的蛇毒C - 型凝集素样蛋白的α亚基相似。序列同源性比较并结合半胱氨酸位点分析, 推测DRS2L1 和DRS2L2 可能分别是圆斑蝰蛇毒Ⅹ因子激活剂的轻链LC2 和LC1 。DRS2L3 和DRS2L4 可能是高分子量的蛇毒C - 型凝集 素样蛋白的β亚基, 而DRS2L5 和DRS2L6 可能是低分子量的蛇毒C - 型凝集素样蛋白的β亚基。DRS2L7 可能是 类似于血小板膜糖蛋白Ib 结合蛋白的β亚基。