阿尔茨海默氏病大鼠海马内植入神经干细胞后效果观察

目的：观察神经干细胞植入阿尔茨海默氏病（AD）大鼠海马内的存活和增殖情况,以及对学习记忆能力的影响一方法：从新生大鼠海马齿状回分离、培养神经干细胞,经Hoechst33258标记后植入AD模型大鼠海马,2周和4周后,行Y迷宫实验检测大鼠的学习记忆能力,然后取脑进行荧光观察和PCNA免疫组织化学染色。结果：与AD组相比,2周移植组和4周移植组大鼠的学习能力和记忆能力有明显提高一移植的神经干细胞能在海马存活,与周围组织建立良好的整合,还可沿海马CAl区迁移,而且在海马CAl区内可见许多PCNA阳性细胞：结论：新生大鼠海马齿状回神经干细胞移植到AD大鼠海马内能够存活、增殖,并能改善AD大鼠的学习能力和记忆能力。     

小檗碱对血管性认知功能障碍模型大鼠学习记忆能力的影响*

目的:观察小檗碱(berberine)对血管性认知功能障碍(VCI)大鼠学习记忆的影响。 方法:68只Wistar大鼠随机分为:正常组10只、 假手术组10只、造模组48只。造模组大鼠行双侧颈动脉结扎术制备血管性认知功能障碍模型,造模后大鼠又随机分为血管性认知功能障模型组、小檗碱低剂量(20 mg/kg)组、中剂量(40 mg/kg)组和高剂量(60 mg/kg)组(每组大鼠10只)。治疗组腹腔注射不同剂量的小檗碱,其余组腹腔注射生理盐水,每天1次,共34 d。给药28 d后,Morris水迷宫检测大鼠学习记忆能力;水迷宫实验后,检测超氧化物歧化酶(SOD)活性和谷胱甘肽(GSH)、丙二醛(MDA)以及前脑皮层TNF-α、IL-1β、5-HT的含量与单胺氧化酶(MAO)的含量。 结果:与假手术组比较,模型组大鼠逃避潜伏期显著延长(P＜0.01),通过平台次数显著减少(P＜0.01),海马或前脑皮层SOD、GSH和5-HT水平明显降低(P＜0.01),MDA、TNF-α、IL-1β和MAO水平明显升高(P＜0.01);与模型组相比,小檗碱各治疗组逃避潜伏期显著缩短(P＜0.01,P＜0.05),通过平台的次数显著增加(P＜0.01,P＜0.05),海马或前脑皮层SOD、GSH 和5-HT水平明显升高(P＜0.01),MDA、TNF-α、IL-1β和MAO水平明显降低(P＜0.01)。结论:小檗碱显著提高血管性认知功能障碍模型大鼠的空间学习记忆能力,其机制可能与小檗碱调节大鼠的海马抗氧化应激、抗炎性反应和前脑皮层单胺类神经递质系统的作用有关。小檗碱60 mg/kg组作用较好。     

Energetic cost of learning and memory can cause cognitive impairment in honeybees

The energetic cost of cognitive functions can lead to either impairments in learning and memory, or to trade-offs with other functions, when the amount of available energy is limited. However, it has been suggested that, under such conditions, social groups such as honeybees might be able to ward off cognitive impairments in individual bees by adjusting resource allocation at the colony level. Using two complementary experiments, one that tests the effect of learning on subsequent energetic state and survival, and another that tests the effect of energetic state on learning and retention, we show that individual bees pay a significant energetic cost for learning and therefore suffer from significant cognitive deficits under energetic stress. We discuss the implications of such cognitive impairments for the recent observations of bees disappearing from their colonies as well as for social life in general.     

Dopamine induces release of calcium from internal stores in layer II lateral entorhinal cortex fan cells.

The entorhinal cortex plays an important role in temporal lobe processes including learning and memory, object recognition, and contextual information processing. The alteration of the strength of synaptic inputs to the lateral entorhinal cortex may therefore contribute substantially to sensory and mnemonic functions. The neuromodulatory transmitter dopamine exerts powerful effects on excitatory glutamatergic synaptic transmission in the entorhinal cortex. Interestingly, inputs from midbrain dopamine neurons appear to specifically target clusters of excitatory cells located in the superficial layers of the entorhinal cortex. We have previously demonstrated that dopamine facilitates synaptic transmission through the activation of D₁-like receptors. This facilitation of synaptic transmission is dependent on both activation of classical D₁-like-receptors, and upon activation of dopamine receptors linked to increases in phospholipase C, inositol triphosphate (IP₃), and intracellular calcium. In the present study we combined electrophysiological recordings of evoked excitatory postsynaptic currents with imaging of intracellular calcium using the fluorescent indicator fluo-4 to monitor calcium transients evoked by dopamine in electrophysiologically identified putative fan and pyramidal cells of the lateral entorhinal cortex. Bath application of dopamine (1 μM), or the phosphatidylinositol (PI)-linked D₁-like-receptor agonist SKF83959 (5 μM), induced reliable and reversible increases in fluo-4 fluorescence and excitatory postsynaptic currents in fan cells, but not in pyramidal cells. In contrast, application of the classical D₁-like-receptor agonist SKF38393 (10 μM) did not result in significant increases in fluorescence. Blocking release of calcium from internal stores by loading cells with the IP₃ receptor blocker heparin (1 mM) or the ryanodine receptor blocker dantrolene (20 μM) abolished both the calcium transients and the facilitation of evoked synaptic currents induced by dopamine. Dopamine also induced calcium transients in fan cells when calcium was excluded from the extracellular medium, further indicating that the calcium transients are linked to release from internal stores. These results indicate that following D₁-like-receptor binding, dopamine selectively induces transient elevations in intracellular calcium via activation of IP₃ and ryanodine receptors, and that these elevations are linked to the facilitation of synaptic responses in putative layer II entorhinal cortex fan cells.     

Nicotine evoked improvement in learning and memory is mediated through NPY Y1 receptors in rat model of Alzheimer's disease

We investigated the role of endogenous neuropeptide Y (NPY) system in nicotine-mediated improvement of learning and memory in rat model of Alzheimer's disease (AD). Intracerebroventricular (icv) colchicine treatment induced AD-like condition in rats and showed increased escape latency (decreased learning), and amnesic condition in probe test in Morris water maze. In these rats, nicotine (0.5mg/kg, intraperitoneal), NPY (100 ng/rat, icv) or NPY Y1 receptor agonist [Leu(31), Pro(34)]-NPY (0.04 ng/rat, icv) decreased escape latency by 54.76%, 55.81% and 44.18%, respectively, on day 4 of the acquisition. On the other hand, selective NPY Y1 receptor antagonist, BIBP3226 (icv) produced opposite effect (44.18%). In the probe test conducted at 24h time point, nicotine, NPY or [Leu(31), Pro(34)]-NPY increased the time spent by 72.72%, 44.11% and 26.47%, respectively; while BIBP3226 caused reduction (8.82%). It seems that while NPY or [Leu(31), Pro(34)]-NPY potentiated, BIBP3226 attenuated the learning and memory enhancing effects of nicotine. Brains of colchicine treated rats showed significant reduction in NPY-immunoreactivity in the nucleus accumbens shell (cells 62.23% and fibers 50%), bed nucleus of stria terminalis (fibers 71.58%), central nucleus of amygdala (cells 74.33%), arcuate nucleus (cells 70.97% and fibers 69.65%) and dentate gyrus (cells 58.54%). However, in these rats nicotine treatment for 4 days restored NPY-immunoreactivity to the control level. We suggest that NPY, perhaps acting via NPY Y1 receptors, might interact with the endogenous cholinergic system and play a role in improving the learning and memory processes in the rats with AD-like condition.     

电针对去卵巢大鼠学习记忆能力及海马神经元型一氧化氮合酶mRNA表达的影响

目的研究电针对去卵巢大鼠学习记忆能力及海马神经元型一氧化氮合酶（nNOS）mRNA表达的影响。方法采用卵巢切除大鼠模型,造成低雌激素记忆障碍,去势2周后进行电针刺激,连续治疗3个月。Morris水迷宫测试空间学习记忆能力,酶联免疫吸附分析（ELISA）检测血清雌二醇（E2）浓度,实时荧光定量PCR检测检测nNOSmRNA的相对表达量。结果与假手术组比较,模型组大鼠逃避潜伏期时间明显延长,跨越平台次数明显减少,血清E2浓度和海马nNOSmR—NA表达显著降低（P〈O．01）;与模型组比较,电针组和假电针组治疗后逃避潜伏期缩短,跨越平台次数增加,血清E2浓度和海马nNOSmRNA表达均显著升高,电针组升高更明显（P〈O．01）。结论电针能够提高去卵巢大鼠学习记忆能力,其机制可能与升高体内雌激素浓度上调海马nNOSmRNA的表达有关。     

Characterisation of learning and memory deficits following NMDA receptor antagonism

Summary The effects of the non-competitive NMDA antagonist dizocilpine in tests of cognitive function have been compared with its effects on motor function in rats. Severe motor impairments were observed at doses above 0.1 mg/kg. Dizocilpine (0.075 mg/kg) had no effect on the acquisition of a spatial discrimination task in a Y-maze, but disrupted reversal learning. Both the acquisition and reversal of a visual discrimination task were impaired following dizocilpine (0.075 mg/kg). Dizocilpine (0.04 mg/kg) also disrupted performance of a fivechoice visual reaction time task. It is clear that dizocilpine can impair cognitive function at doses which do not induce pronounced motor dysfunction. The impairment induced by dizocilpine includes a disruption of spatial discrimination learning and a deficit in tasks with sustained attentional demands.     

Photobiomodulation preconditioning prevents cognitive impairment in a neonatal rat model of hypoxia‐ischemia

Neonatal hypoxia‐ischemia (HI) injury caused by oxygen deprivation is the most common cause of mortality and severe neurologic deficits in neonates. The present work evaluated the preventative effect of photobiomodulation (PBM) preconditioning, and its underlying mechanism of action on brain damage in an HI model in neonatal rats. According to the optimal time response of ATP levels in brain samples removed from normal rats, a PBM preconditioning (PBM‐P) regimen (808 nm CW laser, 1 cm² spot, 100 mW/cm², 12 J/cm²) was delivered to the scalp 6 hours before HI. PBM‐P significantly attenuated cognitive impairment, volume shrinkage in the brain, neuron loss, dendritic and synaptic injury after HI. Further mechanistic investigation found that PBM‐P could restore HI‐induced mitochondrial dynamics and inhibit mitochondrial fragmentation, followed by a robust suppression of cytochrome c release, and prevention of neuronal apoptosis by inhibition of caspase activation. Our work suggests that PBM‐P can attenuate HI‐induced brain injury by maintaining mitochondrial dynamics and inhibiting the mitochondrial apoptotic pathway.      

染料木素对卵巢切除大鼠学习记忆能力的影响

目的：探讨染料木素对卵巢切除大鼠学习记忆能力的影响及作用机制。方法：将40只SD雌性大鼠随机分为用假手术组、去卵巢对照组、染料木素高剂量、低剂量组、17β-雌二醇组,切除卵巢建立学习和记忆能力受损的模型。灌胃给药6周后Morris水迷宫测定各组大鼠学习记忆能力,免疫组化法观察大鼠海马微管相关蛋白（tau蛋白）阳性表达情况,测定大鼠脑组织中乙酰胆碱酯酶（AchE）、乙酰胆碱转移酶（ChaT）、超氧化物歧化酶（SOD）的活性及丙二醛（MDA）的含量,观察海马组织超微结构变化。结果：大鼠切除卵巢后Morris水迷宫测定的学习记忆能力显著下降,微管相关蛋白（tau蛋白）异常磷酸化阳性表达率增高,前脑皮质中超氧化物歧化酶（SOD）、乙酰胆碱转移酶（ChaT）活性降低,丙二醛（MDA）含量、乙酰胆碱酯酶（AchE）活性增高。低剂量的染料木素可以发挥类雌激素样作用,改善去卵巢大鼠的以上症状。结论：染料木素对卵巢切除导致的学习和记忆能力下降有改善作用,低剂量效果显著,其可能的机制是：抑制了脑内AchE的活性,使乙酰胆碱的降解减少;增强脑组织抗氧化能力;稳定微管相关蛋白（tau蛋白）,降低tau蛋白异常磷酸化水平。     

Acetylcholinesterase induces neuronal cell loss,astrocyte hypertrophy and behavioral deficits in mammalian hippocampus

Previous studies have demonstrated that acetylcholinesterase (AChE) promotes the assembly of amyloid-beta-peptides into neurotoxic amyloid fibrils and is toxic for chick retina neuronal cultures and neuroblastoma cells. Moreover, AChE is present in senile plaques in Alzheimer's disease (AD) brains. Here we have studied the effect of AChE on astrocytes and hippocampal neurons in vivo. Morphological as well as behavioral disturbances were analyzed after intrahippocampal injection of AChE. Rats were trained in the Morris water maze and assayed for behavioral parameters. Neuronal cell loss was found in the upper leaf of the dentate gyrus in rats injected with AChE in comparison with control animals. Glial fibrillary acidic protein immunoreactivity showed astrocytic hypertrophy and the magnitude of the response was associated with neuronal cell loss. Behavioral results show that injection of AChE produces cognitive impairment demonstrated by an altered water maze performance including (i) a higher escape latency score, (ii) a decreased spatial acuity and (iii) a shorter time of swimming in the platform quadrant. These findings indicate that a local increment in neuronal AChE concentration at the mammalian hippocampus, such as those present in amyloid deposits, may play a role in triggering neuropathological and behavioral changes such as those observed in AD brains.     

Progression of age-associated cognitive impairment correlates with quantitative and qualitative loss of TrkA receptor protein in nucleus basalis and cortex

A direct correlation between disease progression and reduced expression of TrkA receptor in cholinergic neurons has been documented in neurocognitive pathologies including Alzheimer's disease. We investigated whether reduced expression of TrkA protein might also correlate with the level of cognitive impairment in age-associated cognitive impairment. Quantitative and qualitative measurements of TrkA protein levels in the cortex and nucleus basalis of aged rats that had been well-characterized behaviorally as 'unimpaired', 'mildly impaired' or 'fully impaired' demonstrated significant changes in TrkA expression. In the mildly impaired cognitive state phenotypic silencing of TrkA was detected in neurons expressing TrkA at high density but before cholinergic atrophy or loss of TrkA+ neurons was detected. In the fully impaired cognitive state a significant loss in TrkA+ cholinergic neurons together with a more significant phenotypic silencing of TrkA expression then took place. These data suggest that TrkA+ cholinergic cells are associated with cognition, TrkA could be a biomarker of the cognitive state and phenotypic loss of TrkA precedes neuronal loss and probably sensitizes cells to death. We speculate that neurotrophic deficits may be a shared mechanism for cognitive decline in aging and Alzheimer's disease.     

脂联素改善阿尔茨海默病模型小鼠焦虑情绪及工作记忆

目的：探讨脂联素（APN）预处理对9月龄三转基因阿尔茨海默病（3xTg-AD）模型小鼠学习记忆能力和焦虑情绪的影响。方法：选取9月龄3xTg-AD小鼠及C57BL/6J小鼠,分为4组：WT+Saline组、3xTg-AD+Saline组、WT+APN组和3xTg-AD+APN组,每组8只。将全部小鼠进行侧脑室埋管术后,恢复7 d,在自由清醒状态下分别经侧脑室给予生理盐水或APN,采用旷场、新物体识别及Y-迷宫3种行为学手段检测小鼠的情绪及学习记忆能力。结果：①在旷场实验中,与WT+Saline组小鼠相比,3xTg-AD+Saline组小鼠在中央区域的活动时间明显缩短,在外周区域的活动时间明显延长,给予APN后可有效逆转3xTg-AD小鼠的该现象,表明脂联素可有效缓解3xTg-AD小鼠的焦虑情绪。②新物体识别实验中,3xTg-AD+Saline组小鼠的辨别指数为（-16.7±10.1）%,明显低于WT+Saline组的（18.0±8.2）%（P<0.01）和3xTg-AD+APN组的（15.7±8.8）%（P<0.01）,表明脂联素可明显改善3xTg-AD小鼠的识别记忆能力损伤。③Y-迷宫实验中,3xTg-AD+Saline组小鼠的自发交替正确率为（40.0±1.7）%,明显低于WT+Saline组的（56.6±4.6）%（P<0.01）和3xTg-AD+APN组的（53.9±5.6）%（P<0.01）,表明脂联素能够逆转3xTg-AD小鼠工作记忆能力的损伤。结论：脂联素可以改善9月龄3xTg-AD小鼠的焦虑情绪及识别记忆和工作记忆能力损伤,可能在AD的预防和治疗中发挥有效作用。     

树鼩模型:抑郁症的社会竞争失败与学习和记忆的被捕获条件反射

最近基因组研究表明树鼩属于灵长类或是与灵长类亲缘关系最密切的姐妹种.因此,树鼩可能是应用于建立人类疾病动物模型的最佳动物之一.该文报道一种抑郁症的社会竞争失败病因学树鼩(Tupaia belangerichinensis)模型.一对雄性树鼩被饲养在一个双笼中,用网格把双笼隔开,网格上有一小门.适应1周后,把小门打开,这一对树鼩产生短暂的争斗,每天一次,连续21天.其中争斗失败者被称为服从者.这个过程可导致每天1 h的直接社交冲突和23 h的间接相互影响(比如通过气味、视觉等).与正常对照相比,失败者在第三周也就是社交冲突的最后一周显示了体重、自主活动、躲避行为、尿液皮质醇水平等的变化,并且这种改变可持续至少2周以上.此外,还报道全新的记忆模型,一种被捕获条件反射树鼩模型.在一个封闭的小房间中放置捕获笼,其中挂有一片苹果,小房间中有一只自由活动的树鼩.训练的前4次树鼩进入捕获笼吃苹果并不触发捕获笼关闭,但在第5次时触发捕获笼关闭,并持续一小时才释放树鼩.第1-5次树鼩进入捕获笼的延迟时时间作为适心性指标,其中第5次才是作为被捕获的一次学习训练.24 h后,测试树鼩进入捕获笼的延迟时间作为被捕获记忆能力指标.树鼩经过第5次被捕获训练,能形成很好的被捕获记忆,因为24 h后的延迟时间极人地增加.在训练前腹腔注射已知能阻断记忆形成的NMDA受体拮抗剂MK-801(0.2 mg/kg,腹腔注射),对适应指标没有显著影响,但足极大地缩短了24 h后测试的延迟时间,即阻断了被捕获记忆.这些结果表明了一种抑郁症的慢性社会竞争失败与学习和记忆的一次被捕获条件反射树鼩模型.这两种树趵模型对抑郁症与学习和记忆的机理研究、抗抑郁症新药的临床前药效学评价具有潜在的重要意义.

Abstract：

Recent genome studies indicate that tree shrew is in the order or a closest sister of primates, and thus may be one of the best animals to model human diseases. In this paper, we report on a social defeat model of depression in tree shrew (Tupaia belangeri chinensis). Two male tree shrews were housed in a pair-cage consisting of two independent cages separated by a wire mesh partition with a door connecting the two cages. After one week adaptation, the connecting door was opened and a brief fighting occurs between the two male tree shrews and this social conflict session consisted of 1 h direct conflict (fighting) and 23 h indirect influence (e.g. smell, visual cues) per day for 21 days. The defeated tree shrew was considered the subordinate. Compared with naive animals, subordinate tree shrews at the final week of social conflict session showed alterations in body weight, locomotion, avoidance behavior and urinary cortisol levels.Remarkably, these alterations persisted for over two weeks. We also report on a novel captive conditioning model of learning and memory in tree shrew. An automatic trapping cage was placed in a small closed room with a freely-moving tree shrew. For the first four trials, the tree shrew was not trapped when it entered the cage and ate the bait apple, but it was trapped and kept in the cage for 1 h on the fifth trial. Latency was defined as the time between release of the tree shrew and when it entered the captive cage. Latencies during the five trials indicated adaptation. A test trial 24 h later was used to measure whether the one-trial trapping during the fifth trial could form captive memory. Tree shrews showed much longer trapping latencies in the test trial than the adaptation trials. The N-methyl-d-aspartate (NMDA) receptor antagonist MK-801 (0.2 mg/kg, i.p.), known to prevent the formation of memory, did not affect latencies in the adaptation trails, but did block captive memory as it led to much shorter trapping latencies compared to saline treatment in the test trial. These results demonstrate a chronic social defeat model of depression and a novel one-trial captive conditioning model for learning and memory in tree shrews, which are important for mechanism studies of depression, learning,memory, and preclinical evaluation for new antidepressants.     

茶碱改善东莨菪碱诱发的大鼠记忆障碍

用高效液相色谱测定了不同年龄ＳＤ大鼠与记忆有关脑区的腺苷和乙酰胆碱水平。结果表明,１８～２０月龄鼠的脑内腺苷含量明显高于３～６月龄鼠,而乙酰胆碱（ＡＣｈ）含量却显著低于３～６月龄鼠。经腹腔给大鼠注射东莨宕碱建立近期记忆障碍模型,同时经脑室给予茶碱后,其跳台成绩明显对照组,且脑内ＡＣｈ含量亦显著升高。提示腺苷含量的随龄增加可能是老年记忆障碍的一个重要因素,茶碱作为腺苷受体阻断剂可能通过提高脑内ＡＣｈ     

Role for brain-derived neurotrophic factor in learning and memory

In addition to its actions on neuronal survival and differentiation, brain-derived neurotrophic factor (BDNF) has a role in the regulation of synaptic strength. Long-term potentiation, a form of synaptic plasticity, is markedly impaired in BDNF mutant mice, but the changes were restored by the re-expression of BDNF. BDNF also influences the development of patterned connections and the growth and complexity of dendrites in the cerebral cortex. These results suggest a role for BDNF in learning and memory processes, since memory acquisition is considered to involve both short-term changes in electrical properties and long-term structural alterations in synapses. Memory acquisition is associated with an increase in BDNF mRNA and TrkB receptor activation in specific brain areas. Moreover, the pharmacologic and genetic deprivation of BDNF or its receptor TrkB results in severe impairment of learning and memory in mice, rats and chicks. The effect of BDNF on learning and memory may be linked to the modulation of NMDA and non-NMDA receptor functions as well as the expression of synaptic proteins required for exocytosis. Activation of the mitogen-associated protein kinase and/or phosphatidylinositol 3-kinase signaling pathways may be involved in BDNF-dependent learning and memory formation. It is concluded that BDNF/TrkB signaling plays an important role in learning and memory.     

Delayed injection of neural progenitor cells improved spatial learning dysfunction after cerebral ischemia

Although stem cells are likely to improve neurological deficits seen after cerebral ischemia, the effects of neural progenitor cells (NPCs) on cerebral ischemia-induced learning dysfunction remain to be clarified. We tested whether the delayed injection of exogenous NPCs could prevent learning dysfunction after cerebral ischemia. Cerebral ischemia was produced by the injection of microspheres into the right hemisphere of each rat. Injection of NPCs obtained from green fluorescent protein transgenic rats into the hippocampus on Day 7 after the induction of cerebral ischemia improved the modified neurological severity score and reduced the prolongation of the escape latency seen in the water maze task. A few of the injected NPCs were positive for mature neuronal markers. In addition, the injected NPCs expressed BDNF on Day 28 after cerebral ischemia. Thus, the exogenous NPCs delivered by injection could act as a source of neurotrophic factors and prevent cerebral ischemia-induced learning dysfunction.     

人巨细胞病毒感染对学习记忆影响的研究进展

巨细胞病毒感染可影响儿童的学习记忆能力,是导致儿童智力残疾的主要原因之一。长期以来相关研究主要集中于巨细胞病毒先天性感染对学习记忆的影响及其机制。近年来,越来越多研究也开始关注围生期及获得性巨细胞病毒感染。本综述旨在对近期的巨细胞病毒感染致学习记忆损伤的研究现状加以概括总结。     

The effect of cdk-5 overexpression on tau phosphorylation and spatial memory of rat

In Alzheimer’s disease (AD), hyperphosphorylation of tau may be the underlying mechanism for the cytoskeletal abnormalities and neuronal death. It was reported that cyclin-dependent kinase5 (cdk-5) could phosphorylate tau at most AD-related epitopesin vitro. In this study, we investigated the effect of cdk-5 overexpression on tau phosphorylation and spatial memory in rat. We demonstrated that 24 h after transfection into rat hippocampus, cdk-5 was overexpressed and induced a reduced staining with antibody tau-1 and an enhanced staining with antibodies 12e8 and PHF-1, suggesting hyperphosphorylation of tau at Ser199/202, Ser262/356 and Ser396/404 sites. Additionally, the cdk-5 transfected rats showed long latency to find the hidden platform in Morris water maze compared to the control rat. 48 h after transfection, the level of cdk-5 was decreased significantly, and the latency of rats to find the hidden platform was prolonged. It implies thatin vivo overexpression of cdk-5 leads to impairment of spatial memory in rat and tau hyperphosphorylation may be the underlying mechanism.     

Role of ghrelin system in neuroprotection and cognitive functions: implications in Alzheimer's disease

Alzheimer's disease (AD) is a multifactorial progressive neurodegenerative disorder characterized by loss of memory and cognitive deficits, strongly influenced by the metabolic status, in which the impairment of neuropeptides/neurotransmitters systems has been previously observed. Ghrelin is a multifunctional hormone produced in a wide variety of tissues, which has been associated with the progression of obesity and metabolic syndrome, but has been also linked to neuromodulation, neuroprotection and memory and learning processes. In addition, ghrelin system also acts in an autocrine/paracrine fashion where the majority of its components [ghrelin variants (native ghrelin, In1-ghrelin), acylation enzyme (GOAT) and receptors (GHS-Rs)] are expressed in the different regions of central nervous system. In spite of all these pieces of information strongly suggesting a close association between ghrelin system and AD, which could be of pathophysiological relevance, few studies have been addressed to clarify this relationship. In this work, the role of ghrelin system in neuroprotection, memory consolidation and learning is reviewed, and its influence in AD, as well as the regulation of its expression in the brain of AD patients, is discussed.     

交通噪音对中缅树鼩行为、学习记忆和氧化应激的影响

为探讨噪音刺激对中缅树鼩行为、学习记忆和氧化应激的影响,将中缅树鼩在噪音0 dB、40 dB和80 dB条件下持续刺激8h,连续28 d,测定其体重、摄食量、Y型迷宫正确反应率和行为变化,并测定脑中丙二醛(Malondialdehyde,MDA)、超氧化物歧化酶(Superoxide dismutase,SOD)、乙酰...