根茎在羊草响应短期盐胁迫和干旱胁迫过程中的作用

羊草 (Leymus chinensis (Trin.) Tzvel.) 又称碱草，隶属禾本科，赖草属，因其营养价值高，富含蛋白质，适口性好，抗旱，耐盐碱，耐贫瘠，抗逆性强，适应广等优点，对我国发展草原畜牧业和退化草地、荒漠化治理方面具有举足轻重的作用。近年来，由于自然环境变劣，荒漠化加剧，以及过渡放牧等不利影响，已对我国草地构成了严重威胁，严重制约了我国人工草地建设和天然草地的改良和沙化治理的步伐。目前, 国内外关于羊草的报道大多集中在草原生态等宏观领域，在羊草根茎生理学方面的研究却十分匮乏。作为一种典型的根状茎型克隆植物，羊草根茎在无性繁殖和克隆基株间的克隆整合、形态可塑性和分工合作等方面具有重要的作用,但羊草根茎在羊草感应环境胁迫中的作用却研究甚少。为了探讨根茎在植物感应环境胁迫中的作用, 本文以羊草为实验材料，通过分别处理羊草根茎和根，研究和比较了短期NaCl、PEG胁迫根、根茎、根和根茎三种处理方式下羊草对盐胁迫和干旱胁迫的生理响应。主要研究结果如下： 1、200 mmol• L-1 NaCl处理羊草根、根茎、根和根茎24小时显著降低羊草叶片净光合速率和蒸腾速率，增加叶片渗透浓度与脯氨酸含量;其中同时处理根和根茎，叶片蒸腾速率和净光合速率的降低程度显著高于分别处理根和根茎。在分别处理根与根茎的情况下，叶片含水量、脯氨酸含量、净光合速率、蒸腾速率均无显著性差异。不论单独胁迫根、根茎还是同时胁迫根和根茎，羊草根、根茎和叶片内钠离子（Na+）含量增加，而钾离子（K+）含量和K+/Na+ 比降低。 这些结果表明：（1）羊草根茎在感应和响应盐胁迫的生理过程中与根系具有类似的功能;（2）羊草根茎在盐胁迫条件下参与Na+ 吸收和向地上部的转运;（3）鉴于根茎的生物量和表面积都明显的低于根系，在盐胁迫下羊草根茎吸收Na+ 的效率高于根系。 2、15％ 聚已二醇（PEG－6000）处理羊草根、根茎、根和根茎24 小时显著降低羊草叶片含水量、净光合速率、蒸腾速率和水分利用效率，增加叶片脯氨酸含量。在分别胁迫根与根茎两种处理下，处理根茎对叶片的净光合速率影响程度更大，表明根茎对干旱胁迫反应更敏感。

PEG引发预防大豆种子吸胀冷害的研究

黑河3号大豆种子对低温吸胀非常敏感，PEG引发处理明显提高抗吸胀冷害能力。引发处理的效果与引发后种子含水量的提高有关。引发3天种子含水量达到34%左右。 引发处理过程中种子呼吸强度提高，呼吸商大于1。引发3天大豆种子胚根细胞ATP酶活性定位于质膜、细胞壁及细胞间隙。 引发种子和对照种子低温吸胀后，在常规增减条件下生理生化过程有显著的不同，这些差异与二者不同的种子活力水平有关。引发种子浸种过程中细胞物质损失少，膜选择性通透能力强。对照种子有大量物质外渗，特别是K+。引发种子常规培养条件下呼吸强度上升很快，RQ较低。对照种子呼吸强度很低。引发种子线粒体以L－Mal、α－Kg和Succ为底物时，具有较高的ADP／O和RC，并且氧化磷酸化活性出现早。对照种子线粒体氧化磷酸化功能不健全。引发种子胚根细胞ATP酶活性定位于质膜、核仁、胞间连丝及液泡膜。对照种子ATP酶活性在各亚细胞结构大为降低。 本文讨论了吸胀冷害的普遍性以及吸胀冷害对农业生产的影响，并推论低温吸胀主要导致敏感种子吸胀初期正在进行结构转化的膜系统不可逆损伤从而种子活力下降。PEG引发处理具有防止低温吸胀时膜系统伤损和修复种子成熟、加工、干燥贮藏阶段损伤的作用。PEG引发还预先活化了种子代谢系统。从而使种子萌发迅速、整齐，显著地提高敏感种子搞吸胀冷害能力，对于不存在吸胀冷害问题的种子，PEG引发也有提高种子活力的效果。

Enriched environment treatment counteracts enhanced addictive and depressive-like behavior induced by prenatal chronic stress

Prenatal stress can cause many long-term behavior changes in offspring, but whether prenatal stress can alter addictive behavior in offspring and postnatal enriched environment treatment (EE) can restore these changes are unknown. We reported here that pr

Both stress experience and age determine the impairment or enhancement effect of stress on spatial memory retrieval

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.

Effect of paradoxical sleep deprivation and stress on passive avoidance behavior

Previous studies have shown that several types of stress can induce memory impairment. However, the memory effects of paradoxical sleep deprivation (PSD), a stressor in itself, are unclear. We therefore compared passive avoidance behavior of rats undergoing PSD and PSD stress yoked-control (PSC) using the "reversed flowerpot method." When rats were kept isolated on a PSC platform for 24 It immediately after criterion training, retention trials showed impaired aversive memory storage. When delayed for 24 h after criterion training, PSC stress did not disrupt retention performance. In rats subjected to PSD, either immediately or 24 It after criterion training, there was no disruption of aversive memory consolidation. These results suggest that, during stress, paradoxical sleep plays a role in erasing aversive memory traces, in line with the theory that we "dream in order to forget." (C) 2003 Elsevier Inc. All rights reserved.

Environmental enrichment and chronic restraint stress in ICR mice: Effects on prepulse inhibition of startle and Y-maze spatial recognition memory

In most studies regarding the improving or therapeutical effects induced by enriched environment (EE), EE was performed after the stress treatment or in patients with certain diseases. In the current study, the effects of chronic restraint stress (6 h/day) in mice living in an enriched environment or standard environment (SE) were tested. Mice were randomly divided into 4 groups: non-stressed or stressed mice housed in SE or EE conditions (SE, stress + SE, EE, stress + EE). Prepulse inhibition (PPI) of startle was tested after the 2 weeks or 4 weeks stress and/or EE treatment and 1 or 2 weeks withdrawal from the 4 weeks treatment. After the 4 weeks treatment, spatial recognition memory in Y-maze was also tested. The results showed that EE increased PPI in stressed and non-stressed mice after 2 weeks treatment. No effect of EE on PPI was found after the 4 weeks treatment. 4 weeks chronic restraint stress increased PPI in mice housed in standard but not EE conditions. Stressed mice showed deficits on the 1 h delay version of the Y-maze which could be prevented by living in an enriched environment. Our results indicated that living in an enriched environment reversed the impairing effects of chronic restraint stress on spatial recognition memory. However, EE did not change the effects of stress on PPI. (C) 2010 Elsevier B.V. All rights reserved.

The stress experience dependent long-term depression disassociated with stress effect on spatial memory task

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.

Stress-facilitated LTD induces output plasticity through a synchronized-spikes and spontaneous unitary discharges the CA1 region of the hippocampus

Long-term potentiation (LTP) and long-term depression (LTD) of the excitatory synaptic inputs plasticity in the hippocampus is believed to underlie certain types of learning and memory. Especially, stressful experiences, well known to produce long-lasting strong memories of the event themselves, enable LTD by low frequency stimulation (LFS, 3 Hz) but block LTP induction by high frequency stimulation (HFS, 200 Hz). However, it is unknown whether stress-affected synaptic plasticity has an impact on the output plasticity. Thus, we have simultaneously studied the effects of stress on synaptic plasticity and neuronal output in the hippocampal CA1 region of anesthetized Wistar rats. Our results revealed that stress increased basal power spectrum of the evoked synchronized-spikes and enabled LTD induction by LFS. The induction of stress-facilitated LTD but not LFS induced persistent decreases of the power spectrum of the synchronized-spikes and the frequency of the spontaneous unitary discharges; However, HFS induced UP in non-stressed animals and increased the power spectrum of the synchronized-spikes, without affecting the frequency of the spontaneous unitary discharges, but HFS failed to induce UP in stressed animals without affecting the power spectrum of the synchronized-spikes and the frequency of the spontaneous unitary discharges. These observations that stress-facilitated LTD induces the output plasticity through the synchronized-spikes and spontaneous unitary discharges suggest that these types of stress-related plasticity may play significant roles in distribution, amplification and integration of encoded information to other brain structures under stressful conditions. (C) 2004 Elsevier Ireland Ltd and The Japan Neuroscience Society. All rights reserved.

Gibbons under seasonal stress: the diet of the black crested gibbon (Nomascus concolor) on Mt. Wuliang, Central Yunnan, China

The diet of a habituated group of black crested gibbon (Nomascus concolor jingdongensis) was studied from March 2005 to April 2006 in the Wuliang Mountains, central Yunnan, China. Gibbons consumed 77 different plant species, one mammal-, two bird-, one li

Stress and long-term synaptic depression

Acute inescapable stress reverses the direction of synaptic plasticity in the intact hippocampus via a corticosterone-mediated activation of glucocorticoid receptors and protein/RNA synthesis.

Glucocorticoid receptor and protein/RNA synthesis-dependent mechanisms underlie the control of synaptic plasticity by stress

Learning and memory are exquisitely sensitive to behavioral stress, but the underlying mechanisms are still poorly understood. Because activity-dependent persistent changes in synaptic strength are believed to mediate memory processes in brain areas such as the hippocampus we have examined the means by which stress affects synaptic plasticity in the CA1 region of the hippocampus of anesthetized rats, Inescapable behavioral stress (placement on an elevated platform for 30 min) switched the direction of plasticity, favoring low frequency stimulation-induced decreases in synaptic transmission (long-term depression, LTD), and opposing the induction of long-term potentiation by high frequency stimulation, We have discovered that glucocorticoid receptor activation mediates these effects of stress on LTD and longterm potentiation in a protein synthesis-dependent manner because they were prevented by the glucocorticoid receptor antagonist RU 38486 and the protein synthesis inhibitor emetine. Consistent with this, the ability of exogenously applied corticosterone in non-stressed rats to mimic the effects of stress on synaptic plasticity was also blocked by these agents, The enablement of low frequency stimulation-induced LTD by both stress and exogenous corticosterone was also blocked by the transcription inhibitor actinomycin D, Thus, naturally occurring synaptic plasticity is liable to be reversed in stressful situations via glucocorticoid receptor activation and mechanisms dependent on the synthesis of new protein and RNA, This indicates that the modulation of hippocampus-mediated learning by acute inescapable stress requires glucocorticoid receptor-dependent initiation of transcription and translation.