黄芪注射液在整体抗疲劳实验中对小鼠骨骼肌HK的影响

目的：研究不同剂量的黄芪注射液对小鼠骨骼肌的抗疲劳效应及对肌己糖激酶活性的影响.方法：记录小鼠腓肠肌收缩曲线,测定肌疲劳的时间,检测腓肠肌己糖激酶的活性.结果：与对照组比较,各黄芪注射液组小鼠的肌疲劳的时间均延长,差异具有显著性（P＜0.05）.对照组、黄芪注射液1.2g·kg-1、1.6g·kg-1和2.0g·kg-1组HK活性分别为：5.23±0.87、3.21±1.31、4.68±1.36和4.37±1.52.与对照组比较,黄芪注射液1.2g·kg-1组的HK活性降低,差异具有显著性（P＜0.05）;黄芪注射液1.6g·kg-1和2.0g·kg-1组的HK活性降低,但差异不具有显著性（P＞0.05）.结论：黄芪注射液1.2g·kg-1组具有延缓肌疲劳时间,可适度抑制骨骼肌HK活性而产生抗骨骼肌疲劳效应的作用.     

Effect of growth hormone on memory in mice

In order to determine the effects of growth hormone (GH) on long term memory, two experiments were carried out, all involving a common paradigm. Mice were given massed training on a discrimination task and were injected with GH or control substances before and/or after training: retention was measured 4 weeks later. In Experiment 1, different groups of mice were injected with either GH or saline at five different time points relative to original learning (OL): 90, 30, and 5 min before, and 5 and 30 min after. The results showed a significant quadratic trend, in the form of a U-shaped curve for the GH-injected groups at retention. Maximal retention was observed at the 90 min pre-OL and the 30 min post-OL injection groups. Poorest retention was shown by the 5 min pre-OL injection group. In Experiment 2, GH, saline, and thyroid-stimulating hormone (TSH) were administered at 90 and 5 min pre-OL. In addition, a "state dependency" hypothesis was tested using additional groups of mice. The results again showed a severe drop in retention when GH was administered 5 min before OL; differences between the two pre-OL GH injection groups were less marked than in Experiment 1; TSH did not have the same action as GH; and finally, a state dependency interpretation was ruled out. Together the two experiments present results that indicate a selectively GH-induced suppression of memory when GH is administered in close proximity to OL. As the time lapse between the injection of drug and the learning task increases, the inhibitory effect on memory is reversed.     

Effect of diagnostic ultrasound during the fetal period on learning and memory in mice

BACKGROUND: An experiment was conducted to find out whether in utero exposure to diagnostic ultrasound leads to changes in postnatal behavior in adult mice. METHODS: A total of 15 pregnant Swiss albino mice were exposed to diagnostic levels of ultrasound (3.5 MHz, 65 mW/cm(2), intensity((spatial peak-temporal peak)) (I(SPTP))=1 mW/cm(2), intensity((spatial average-temporal average)) (I(SATA))=240 mW/cm(2)) for 30 min on day 14 or 16 of gestation. All exposed as well as control animals were left to complete gestation and parturition. Their offspring were used in our further studies. They were monitored during early postnatal life for standard developmental markers (such as pinna detachment, eye opening and fur development) and postnatal mortality was recorded up to 6 weeks of age. The litters were subjected to behavioral tests for learning and memory at 4 months of age. Representative animals from each group were sacrificed and the hippocampal region of the brain was assayed for biogenic amines, noradrenaline, dopamine, serotonin (5-HT) and 5-HT's metabolite, 5-hydroxy indoleacetic acid (5-HIAA), in order to determine whether ultrasound exposure produced any biochemical changes in the hippocampal region of the brain. Coronal sections from the dorsal hippocampus from the representative animals from each group were processed for staining and the number of neurons was counted. RESULTS: Neither the standard developmental markers (such as pinna detachment, eye opening and fur development) nor the postnatal mortality was affected by ultrasound exposure. However, there was a significant impairment in learning (hole board test) and memory functions (shuttle box test) in both the exposure groups. Significant reductions in the biogenic amines and the decrease in the neuronal density were found only in day 14th pc ultrasound-exposed group compared with the control animals. The 16th day exposure group is relatively resistant to ultrasound-induced impairment of brain functions. CONCLUSIONS: The results suggest that the early fetal brain is highly susceptible to induction of neurobehavioral changes by ultrasound exposure.     

孕期丰富环境对子代小鼠学习记忆功能的影响

目的探讨雌性小鼠孕期给予丰富环境刺激对子代新生小鼠空间学习记忆能力的影响。方法选择SPF级C57BL／6受孕雌鼠24只随机分为丰富环境组和标准环境组,在整个孕期分别给予丰富环境、普通环境的刺激直至分娩为止。两组小鼠出生后均移至普通环境饲养,在出生后的1个月及2个月时分别对子代小鼠进行水迷宫行为学检测、海马区新生神经元的免疫荧光检测。结果在1月龄的子代小鼠中,定位航行实验显示丰富环境组比普通环境组小鼠的平均逃避潜伏期时间明显缩短（P〈0．05）,而空间探索实验显示丰富环境组平台象限游泳距离百分比和穿台次数均高于普通环境组（P〈0．05）。在海马CA1区和齿状回,丰富环境组神经元前体细胞标记物微管相关蛋白Doublecortin（DCX）阳性神经细胞数目较普通环境组明显增多（P〈0．05）。而在2月龄的子代小鼠检测中,两组小鼠在上述指标均无明显统计学差异。结论在母鼠妊娠期间给予丰富环境刺激可以一过性提高子代小鼠的学习记忆能力以及神经发生发育。     

Effect of lithium on morphine state-dependent memory of passive avoidance in mice

In the present study, effects of lithium chloride (LiCl) on morphine induced state-dependent memory of passive avoidance task were examined in mice. One-trial step-down paradigm was used for the assessment of memory retention in adult male NMRI mice. Administration of morphine (5 mg/kg) subcutaneously (s.c.) 30 min before training or testing induced impairment of memory performance. Injection of the same dose of the drug 30 min before testing restored memory retention impaired under pre-training morphine effect. Intraperitoneal (i.p.) injection of lithium, 60 min before training or prior to testing also impaired memory performance. Under the pre-training of morphine, the response of the opioid was restored when animals received LiCl (80 and 160 mg/kg) as pre-test injection. Pre-training administration of lower dose of lithium (20 mg/kg), but not the higher doses of the drug (80 and 160 mg/kg) impaired memory retention in passive avoidance test. LiCl-induced impairment of memory retention was restored by pre-test administration of morphine. In the animals receiving pre-training morphine, combined pre-test morphine and LiCl administration increased the restoration of memory by the opioid. It can be concluded that there may be a cross-state dependency between morphine and lithium.     

Effect of kami-untan-to on the impairment of learning and memory induced by thiamine-deficient feeding in mice

We have recently reported that thiamine deficient (TD) mice show an impairment of learning and memory on the 20th day after start of TD feeding. Interestingly, it has been reported that the kampo medicine, "kami-untan-to" (KUT) may be useful as a potential therapeutic agent in diseases associated with cholinergic deficit such as Alzheimer's disease. In the present study, we investigated the effects of KUT on the impairment of memory-related behavior concomitant with psychoneuronal symptoms after TD feeding in mice. Oral administration of KUT had no effect on the food intake, body weight or locomotor activity in TD mice, but the mortality rate in the KUT-treated TD group was significantly lower compared with that in the non-treated TD group. Daily administration of KUT from the 1st day of TD feeding protected against the impairment of memory-related behavior induced by TD. The intensity of the choline acetyltransferase fluorescence decreased in the field of CA1 and dentate gyrus in the hippocampus in TD mice compared with pair-fed mice as the control group, and KUT treatment inhibited this decrease. These results suggest that the effect of KUT on the impairment of memory-related behavior induced by TD feeding may be closely related to the activation of cholinergic neurons in the hippocampus.     

TAK-242对脂多糖诱导的脓毒症脑病小鼠学习记忆功能障碍的改善作用

目的:探究TAK-242对脂多糖诱导的脓毒症脑病小鼠学习记忆功能障碍的改善效果,观察小鼠大脑病理学形态的改变,并探究起效的相关蛋白通路机制。方法:健康雌性C57BL/6小鼠80只,10～12月龄,体重20～30 g,采用随机数字表法分为4组(n=20):空白对照组(CON组)、TAK-242对照组(TAK组)、脓毒症脑病模型组(LPS组)和TAK-242预处理组(T+L组);取小鼠动脉血及肺脏组织检测外周炎症情况,应用旷场、高架十字和Morris水迷宫实验观察小鼠的行为学变化,后进行免疫组化实验观察海马区小胶质细胞特异性标志物离子钙结合衔接分子1(Iba-1)的形态和数量,最后通过Western blot实验检测海马区NF-κB p65、TLR4、Aβ1-42和p-tau (S396)蛋白的表达情况。结果:与CON组相比,其余各组小鼠动脉血气和肺脏组织没有出现明显炎症改变;LPS组小鼠在旷场中央区活动时间和穿过中央区次数都显著降低(P0.01),进入高架十字开臂次数和探头区探头次数明显减少(P0.05),水迷宫空间探索潜伏期明显延长(P0.05),海马区Iba-1活化数目显著增加(P0.05),NF-κB p65、TLR4、Aβ1-42和p-tau (S396)蛋白表达量明显增加(P0.01)。与LPS组相比,T+L组小鼠在旷场中央区活动时间和穿过中央区次数显著增加(P0.01),进入高架十字开臂次数和探头区探头次数明显增加(P0.05),水迷宫空间探索潜伏期明显缩短(P0.05),海马区Iba-1活化数目显著减少(P0.05),NF-κB p65、TLR4、Aβ1-42和p-tau (S396)蛋白表达量显著降低(P0.05)。结论:TAK-242对脓毒症脑病引起的学习记忆功能障碍具有一定的预防和治疗作用,其作用机制可能与抑制中枢小胶质细胞活化的数目及下调蛋白NF-κB p65、TLR4、Aβ1-42和p-tau (S396)的表达水平有关。     

Effect of cyclosporin A on the induction and activation of B memory cells by thymus-independent antigens in mice

The effect of cyclosporin A on the induction and activation of B memory cells by thymus-independent (TI) antigens was investigated. Studies were carried out in C57BL/6 mice, a strain in which TI.1 trinitrophenyl-lipopolysaccharide (TNP-LPS) and TI.2 dinitrophenyl-(DNP)-Ficoll antigens can elicit a secondary response. Evidence is presented that cyclosporin A does not adversely affect the primary or secondary response to TNP-LPS. In contrast, this fungal metabolite prevents the triggering of virgin B lymphocytes and TNP-LPS-induced memory cells by DNP-Ficoll. Cyclosporin A does not interfere with the generation of hapten-specific B memory cells by TNP-LPS or DNP-Ficoll. These findings are discussed in terms of B cell lineages leading to antibody-forming cell precursors and memory cells.     

神经发生对小鼠学习记忆能力的影响

本研究探讨神经发生对学习记忆能力的影响。选择健康成年昆明小鼠随机分7组,分别为生理盐水对照组,酸性成纤维细胞生长因子(aFGF)高、中、低剂量组,甲氨喋呤(MTX)高、中、低剂量组。使用脑立体定位仪行侧脑室埋管手术及侧脑室微量注射。用Morris水迷宫训练测试其空间学习与记忆能力;腹腔注射5-溴脱氧尿苷(BrdU)后通过免疫组织化学方法来显示Br-dU阳性细胞。结果表明,aFGF各剂量组学习记忆能力均强于生理盐水对照组;MTX高剂量组学习记忆能力显著低于生理盐水对照组。免疫组织化学结果显示aFGF各剂量组齿状回内BrdU阳性细胞数目显著高于对照组;而MTX高剂量组齿状回BrdU阳性细胞较之显著减少。结果提示,aFGF和MTX可能通过促进或抑制齿状回的神经发生,从而影响小鼠的学习与记忆能力。     

吗啡成瘾小鼠对正常小鼠学习记忆力能力的影响

目的:用BALB/C小鼠建立动物模型,观察吗啡成瘾戒断小鼠对其周围的正常小鼠学习记忆能力的影响。方法:将吗啡成瘾戒断小鼠与正常小鼠同笼饲养,然后用Morris水迷宫实验测定正常小鼠的学习记忆能力,应用RT-PCR的方法检测正常小鼠海马中PKCa、GABA分子表达的变化。结果:水迷宫实验证明,与生理盐水组相比,实验组小鼠的学习记忆能力明显降低(P<0.05),海马中PKCa和DABA的表达都明显升高(P<0.05)。     

磷脂酰丝氨酸/茯苓组合对快速老化模型小鼠学习记忆能力的作用及其机制

目的探讨磷脂酰丝氨酸/茯苓组合对快速老化模型小鼠学习记忆的影响和其作用机制。方法选用50只8周龄雄性C-57小鼠随机分为空白组、生理盐水组、磷脂酰丝氨酸组、茯苓组和磷脂酰丝氨酸/茯苓组合组等5组,每组10只,灌胃给药2周,首先通过Morris水迷宫实验检测各组小鼠空间学习记忆能力,其次检测小鼠的原位LTP,最后取脑组织进行HE染色和基因枪Di I染色。结果与空白组相比,磷脂酰丝氨酸组、茯苓组和磷脂酰丝氨酸/茯苓组合组的学习记忆能力均有所提高,LTP增幅提高,海马CA1区神经元数目增多,神经元树突棘的密度增加,其中磷脂酰丝氨酸/茯苓组合组效果最为明显。结论磷脂酰丝氨酸/茯苓组合能提高快速老化模型小鼠学习记忆能力,其机制可能与保护神经元有关。     

磷脂酰丝氨酸/陈皮组合对快速老化模型小鼠学习记忆能力的作用及其机制

目的:探讨磷脂酰丝氨酸/陈皮组合对快速老化模型小鼠学习记忆的影响及其作用机制。方法:选用8周龄雄性SAM-P8小鼠,随机分为空白组、生理盐水组、磷脂酰丝氨酸组、陈皮组和磷脂酰丝氨酸/陈皮组合组5组,灌胃给药2周。首先通过Morris水迷宫实验检测各组小鼠空间学习记忆能力,其次检测小鼠的原位长时程增强(LTP),最后取脑组织行尼氏染色和基因枪DiI染色。结果:与空白组相比,磷脂酰丝氨酸组、陈皮组和磷脂酰丝氨酸/陈皮组合组的学习记忆能力有所提高,LTP增幅提高,海马CA1区神经元数目增多,神经元树突棘的密度增加,其中磷脂酰丝氨酸/陈皮组合组效果最为明显。结论:磷脂酰丝氨酸/陈皮能提高快速老化模型小鼠学习记忆能力,其机制可能与保护神经元有关。     

卡托普利对小鼠学习记忆能力具有促进作用

目的:研究实验小鼠经卡托普利给药后,小鼠的学习记忆能力的变化及海马区多聚唾液酸神经细胞黏附因子(polysialylated neural cell adhesion molecule,PSA-NCAM)的表达情况。方法:BALB/c小鼠随机分为给药组和对照组,各6只。给药组小鼠腹腔注射卡托普利,每日30 mg/kg,连续7 d;对照组注射等量的无菌生理盐水。给药后对小鼠进行Morris水迷宫试验检测小鼠的学习记忆能力,后取脑切片进行PSA-NCAM免疫组织化学染色。结果:给药组小鼠逃避潜伏期较对照组缩短,而目标象限停留时间及经过平台次数较对照组增加(P0.05)。免疫组织化学法显示两组小鼠海马区PSA-NCAM表达没有明显差异。结论:对实验小鼠给药卡托普利可促进小鼠学习记忆能力,但该药对小鼠海马区PSA-NCAM表达没有明显作用。     

左旋肉碱抗疲劳实验研究

目的研究左旋肉碱抗疲劳的效果。方法将健康雄性昆明小鼠80只随机分入四个组：实验前肌糖原和肝糖原测定组、负重游泳组、血乳酸测定组、尿素氮测定组,每个实验各20只小鼠。每个组再随机分成对照组和实验组,每组10只。对照组每天以蒸馏水灌胃,实验组以600mg/kg左旋肉碱灌胃,连续6周后分别测定肝糖原、肌糖原、游泳时间、血乳酸、血清尿素氮含量等指标,观察左旋肉碱抗疲劳效果。结果左旋肉碱组小鼠游泳时间和运动前肌肝糖原含量较对照组明显增加（P〈0.05）,游泳30min和游泳60min的肌肝糖原消耗均较对照组明显减少（P〈0.05）,力竭游泳后肝糖原消耗较对照组显著减少（P〈0.05）,但肌糖原消耗与对照组比较差异无统计学意义（P〉0.05）;运动后左旋肉碱组乳酸增加较对照组明显降低（P〈0.05）,休息30mim后血乳酸含量较对照组降低,恢复率明显增加（P〈0.05）;运动结束休息60min后左旋肉碱组血清尿素氮增量与对照组比较差异无统计学意义（P〉0.05）,但休息120min后,左旋肉碱组血清尿素氮含量较对照组明显降低,恢复率显著增高（P〈0.05）。结论左旋肉碱具有抗疲劳作用,其抗疲劳作用机理主要与左旋肉碱增加肌肝糖原储备,减少运动后肌肝糖原消耗,抑制乳酸生成,加速乳酸和尿素氮清除有关。     

宫内缺氧对成年小鼠学习记忆能力的影响

目的:探讨孕鼠宫内缺氧对成年小鼠学习记忆能力的影响。方法:用低张性缺氧模型致胎龄13、15、17d小鼠宫内缺氧,新生鼠P1、P7、P14、P28、P90脑组织作Nissl染色,观察海马CA3区锥体细胞层神经元数目及形态,P90小鼠行Morris水迷宫实验。结果:与正常组比较,宫内缺氧组小鼠海马CA3区锥体细胞层神经元数量明显减少,逃避潜伏期延长及穿环次数明显减少。结论:宫内缺氧导致小鼠海马CA3区锥体细胞层神经元数目减少及成年小鼠学习记忆能力降低。     

睡眠剥夺对吗啡成瘾小鼠学习记忆能力的影响

目的:观察睡眠剥夺对吗啡成瘾小鼠的空间学习记忆能力的影响。方法:ICR小鼠40只随机分为4组(n=10):生理盐水对照组、吗啡成瘾实验组、生理盐水+睡眠剥夺对照组、吗啡成瘾+睡眠剥夺实验组。小鼠递增注射吗啡7 d建立成瘾模型后,通过睡眠剥夺箱48 h建立睡眠剥夺模型,水迷宫实验观察其学习记忆的前后差异对比。结果:与单纯吗啡成瘾组及睡眠剥夺组相比,吗啡成瘾+睡眠剥夺组与睡眠剥夺小鼠水迷宫逃避潜伏期时间明显延长(P<0.05)。结论:睡眠剥夺加重吗啡成瘾ICR小鼠的学习记忆能力的损害作用。     

孕酮抗氧化作用对去卵巢小鼠学习记忆能力的影响

目的观察孕酮与小鼠学习记忆功能的维持和改善是否存在相关性,并探讨其机制。方法60只雌性昆明小鼠随机分为5组,除SHAM组外,其余各组小鼠行双侧卵巢切除术。术后对各组小鼠分别腹腔注射不同剂量孕酮或生理盐水。Morris水迷宫测试训练检测各组小鼠学习记忆能力,随后取脑,检测海马组织的SOD、MDA含量及T-AOC。结果OVX组在若干个测试训练时段其空间学习记忆能力显著较差,而孕酮各剂量组表现较好。海马组织SOD含量:SHAM组和孕酮各计量组均显著较高(P<0.05);MDA含量:SHAM组和HP组显著较低(P<0.05);T-AOC:SHAM组和HP组显著增高(P<0.05)。结论雌、孕激素的缺乏会引起成年雌性小鼠学习记忆能力下降,孕酮的长期补充治疗可以通过组织抗氧化作用,抵抗脂质过氧化反应,提高组织的抗氧化能力,来缓解或改善小鼠学习记忆功能障碍。     

CD226分子对小鼠海马相关恐惧记忆的影响

目的:探讨CD226分子对C57BL/6小鼠恐惧记忆的影响。方法:对野生型(Wild type,WT)小鼠和CD226基因敲除(CD226 knockout,Cd226~(-/-))小鼠进行非伤害性声音刺激和/或不可逃避的足底电击刺激联合匹配训练建立场景性恐惧条件化和线索性恐惧条件化模型,分别检测此两种小鼠在不同恐惧条件化模型中的行为反应,利用僵立时间占总测试时间的百分比来评估小鼠的恐惧程度。结果:(1)在场景性恐惧记忆(即海马相关恐惧记忆)检测中,Cd226~(-/-)小鼠僵立时间占总测试时间百分比明显高于野生型小鼠(P=0.090)。(2)在线索性恐惧记忆(即非海马相关恐惧记忆)检测中,结果无显著差异和趋势(P=0.641)。结论:Cd226~(-/-)小鼠海马相关恐惧记忆能力有增强趋势,提示CD226分子可能参与了小鼠海马相关恐惧记忆的调节。