小鼠对新环境和回避反应的记忆特征：开阔行为避暗实验比较

研究小鼠对新环境和回避反应记忆特点。方法：用开阔和避暗实验，结果：小鼠对开阔环境记忆仅保持４８ｈ，对回避反应记忆持续９６ｈ以上，在开阔和回避反应实验中，小鼠获得记忆所需的学习时分分别为０．５和２ｍｉｎ，东莨菪碱，氯丙嗪，异丙嗪，印防已毒素，咖啡因和戊巴比妥能抑制小鼠回避反应，但小鼠对开阔环境的记忆仅被东莨菪碱和咖啡因阻断。结论：与回避反应相比，小鼠对新环境的记忆表现为易获得，易消退，不易被药物阻断     

丁螺环酮对小鼠主动和被动回避反应的影响

应用小鼠一次性被动回避和穿箱主动回避行为法 ,观察抗焦虑剂丁螺环酮 (Bus)对学习获得和记忆保持的影响 .结果发现 ,训练前 ip Bus0 .3- 1 0mg·kg-1不影响小鼠一次性被动回避反应的获得 ,但训练后立即 ip Bus 0 .3- 1 mg· kg-1时损害其保持 ,缩短小鼠进入暗室的潜伏期 .每天训练前 ipBus 0 .3- 1 0 mg· kg-1时 ,小鼠 d 1穿箱主动回避反应率显著提高 ,但随后的 d2 - 4,1 ,3,1 0 mg·kg-1组小鼠主动回避反应率显著降低 .Bus 0 .3-3.0 mg· kg-1不影响小鼠自发活动 ,1 0 mg· kg-1使小鼠活动性降低 ,这些结果表明 Bus不影响或促进学习获得 ,对记忆的保持具有损害作用     

莨菪类生物碱对18,28及38日龄小鼠的行为和记忆障碍作用

比较阿托品（Ａｔｒ），东莨菪碱（Ｓｃｏ），樟柳碱（ＡＴ３）和山莨菪碱（Ａｎｉ）对小鼠行为及记忆损伤作用。方法：行为和记忆实验用开阔和回避反应法。脑Ｍ受体用［＾３Ｈ］ＱＮＢ测定。结果：Ａｔｒ，Ｓｃｏ和ＡＴ３增加小鼠走动行为２６％－４２％，降低站忆。４个药物均能妨碍回避反应。小鼠１８日龄额叶皮层和海马［＾３Ｈ］ＱＮＢ结合位点数少于３８日龄７％－２３％。结论：１）莨菪类生物碱对小鼠行为和记忆障碍的作用随     

Belladonna alkaloids-induced behavioral changes and amnesia on open-field and step-through in 18-,28-, and38-day-old mice

目的：比较阿托品（Ａｔｒ），东莨菪碱（Ｓｃｏ），樟柳碱（ＡＴ３）和山莨菪碱（Ａｎｉ）对小鼠行为及记忆损伤作用．方法：行为和记忆实验用开阔和回避反应法．脑Ｍ受体用［３Ｈ］ＱＮＢ测定．结果：Ａｔｒ，Ｓｃｏ和ＡＴ３增加小鼠走动行为２６％－４２％，降低站立，修饰，排便行为５０％－１００％，并抑制开阔记忆．４个药物均能妨碍回避反应．小鼠１８日龄额叶皮层和海马［３Ｈ］ＱＮＢ结合位点数少于３８日龄７％－２３％．结论：１）莨菪类生物碱对小鼠行为和记忆障碍的作用随其日龄增加而减弱．２）Ｓｃｏ对幼年小鼠的行为及记忆障碍作用的最小有效量分别是Ａｔｒ，ＡＴ３和Ａｎｉ的１／１０，１／１００和１／１０００．     

SNK法及Kruskal-Wallis H检验法研究尼莫地平对小鼠开场行为和学习记忆的影响

采用Ｙ－迷宫分辨学习和一次被动回避反应两种行为模型,利用小鼠海马内微注射技术,检测了钙通道拮抗剂尼莫地平的中枢效应,并观察了开场行为,利用ＳＮＫ法及Ｋｒｕｓｋａｌ－ＷａｌｉｓＨ检验法处理实验数据,结果表明,海马内钙离子水平升高会破坏小鼠的分辨学习能力及一次被动回避反应的记忆保持。尼莫地平本身对正常小鼠的分辨学习无明显影响,但可促进小鼠一次被动回避反应的记忆保持,并可对抗海马内Ｃａ２＋水平升高引起的小鼠分辨学习障碍及记忆保持的破坏。     

中枢注射加压素的促记忆效应

以小鼠为对象,侧脑室内埋植慢性套管,行为训练后icv精氨酸加压素(AVP)1.5 ng/鼠,对抑制性回避反应的记忆保持有增强作用.行为训练前ip肾上腺素β受体阻滞剂Pro 0.5mg/kg,能阻断AVP icv对记忆保持的易化.摘除小鼠双侧肾上腺,不改变外周注射AVP 10μg/kg所产生的促记忆效应.结果提示AVP促记忆作用的部位可能在中枢,并与脑内肾腺β受体有关.     

冰片注射液对小鼠脑缺血再灌注后学习和记忆行为的影响

目的观察冰片对小鼠脑缺血复灌后学习记忆行为的影响。方法采用小鼠夹闭双侧颈总动脉,脑缺血15 min后复灌造模,动物分组给药,人工常规饲养7 d后,检测小鼠跳台错误次数、回避反应和Y型迷宫试验,观察小鼠学习记忆行为的改变。结果冰片可以减少小鼠跳台试验及回避反应中的错误次数,延长Y型迷宫试验中的潜伏期,缩短逃避时间。结论脑缺血复灌损伤可以导致记忆障碍,冰片对小鼠脑缺血后的记忆障碍具有改善作用。     

用跳台法和避暗法观察药物对学习和记忆获得的影响

采用跳台和避暗法，观察康维命（ＣＶＭ）对小鼠学习和记忆获得的影响。结果表明，ＣＶＭ能提高小鼠的学习和记忆获得能力。两种方法均可用于促进学习记忆试验新药品的筛选，跳台法可观察对学习和记忆获得的影响，避暗法仅可观察对记忆获得的影响     

保健食品“脑轻松”改善小鼠学习记忆作用的研究

为研究保健食品“脑轻松”改善记忆功能,选用一组行为学测试方法：水迷宫试验、跳台试验、避暗试验以观察该保健食品对小鼠行为记忆的影响。结果表明,经口给予小鼠０．２、０．４、０．６ｇ／ｋｇ．ｂｗ剂量的受试物３０ｄ,对正常及记忆获得障碍模型小鼠的被动回避反应及空间辨别能力的记忆获得有明显的促进作用。     

中枢烟碱受体亚型对小鼠被动回避行为的影响

目的：探讨中枢烟碱受体亚型在学习、记忆中的作用。方法：采用小鼠的被动回避反应法，观察四种不同选择性的烟碱受体（Ｎ受体）拮抗剂对学习和记忆行为的影响。结果：脑室注射ｋａｐｐａ－银环蛇毒（κ－ＢＴＸ）和六烃季铵（Ｃ６）明显抑制小鼠的学习和记忆行为的获得，且κ－银环蛇毒的作用有量—效关系；而α－银环蛇毒（α－ＢＴＸ）和双氢β－刺酮碱（ＤＨＢＥ）对小鼠的被动回避反应无明显影响。结论：中枢烟碱受体亚型在学习、记忆中起不同的作用，对κ－ＢＴＸ敏感的烟碱受体亚型可能在学习记忆中发挥重要作用。     

异甘草素对丙泊酚致小鼠学习记忆障碍的影响

目的:研究异甘草素(isoliquiritigenin,ISL)对丙泊酚致小鼠学习记忆障碍的影响。方法:选用昆明种小鼠,随机分为5组,每组10只。ISL低、中、高剂量给药组分别灌服ISL 15、30、60mg.kg-1;正常照组和模型组每日灌服等容量的溶媒。灌胃60min后除正常对照组外,其他各组均腹腔注射丙泊酚20mg.kg-1。15min后测试避暗和跳下潜伏期及错误次数(避暗实验和跳台实验),以及10次测试中一次性正确的次数(Y迷宫法)。结果:与正常组比较,模型组避暗和跳下潜伏期缩短,错误次数增加,一次性正确次数减少;与模型组相比,异甘草素可剂量依赖性增加避暗和跳下潜伏期,减少错误次数,增加一次性正确的次数。结论:异甘草素可改善丙泊酚所致小鼠学习记忆障碍。     

胍基琥珀酸促进小鼠学习和记忆的作用(英文)

采用水迷宫实验和一次性被动回避实验 (跳台法和避暗法 ) ,研究了胍基琥珀酸 ( 14,2 8和 56mg·kg- 1,ip)对小鼠学习和记忆的影响 .在水迷宫实验中 ,给小鼠ip胍基琥珀酸 56mg·kg- 1,每日 1次 ,连给 4d ,明显改善小鼠的记忆功能 .无论 1次或连续 4dip上述 3个剂量的胍基琥珀酸对正常小鼠一次性被动回避实验均无明显影响 ,但能明显对抗樟柳碱 ( 5mg·kg- 1,ip) ,亚硝酸钠 ( 12 5mg·kg- 1,sc)和 10 %乙醇 ( 10mL·kg- 1,po)所引起的记忆障碍 .胍基琥珀酸的上述作用近似谷氨酸 ( 30 0mg·kg- 1,ip) .结果表明 ,胍基琥珀酸类似谷氨酸和其他兴奋性氨基酸 ,在调节学习和记忆过程中可能起一定的作用     

咪达唑仑、盐酸戊乙奎醚对小鼠学习记忆的影响

目的观察咪达唑仑、盐酸戊乙奎醚单用、合用对小鼠学习记忆的影响。方法80只昆明(KM)小鼠分层随机区组设计,分为咪达唑仑(1mg.kg-1,midazolan,Mid)组、盐酸戊乙奎醚(0.2mg.kg-1,penehyclidine hydrochloride,Pen)组、咪达唑仑+盐酸戊乙奎醚(1mg.kg-1Mid+0.2mg.kg-1Pen,Mid+Pen)组及生理盐水(10ml.kg-1,NS)组,每组20只;每组再随机分为测试记忆获得组和巩固组,每组10只。采用避暗实验,以训练前/后给药分别评估药物对小鼠记忆获得或巩固的影响。比较各组避暗实验训练后d1、2、3、4、5、6和7测验所得的潜伏期和错误次数。结果①Mid单用或与Pen合用对记忆的获得和巩固均有抑制作用;②Mid合用Pen与Mid单用相比,不加重对记忆获得的抑制,而明显加重对记忆巩固的抑制,且合用比单用抑制记忆时间长。结论Mid和Pen联合使用,对小鼠学习记忆产生明显影响。     

The effect of caffeine in animal models of learning and memory.

In the present investigation we studied the effect of caffeine on memory task inhibitory avoidance and habituation to a new environment. Caffeine impaired retention scores in mice submitted to inhibitory avoidance and habituation when administered 30 min before training at the doses of 10-30 mg/kg. These effects cannot be explained by state-dependency since the administration of caffeine 30 min before the test session did not reverse the effect of pre-training caffeine administration, but can more probably be explained by an impairment in the acquisition or by interference with attentional processes. On the other hand, caffeine improved the inhibitory avoidance (but not habituation) retention scores when administered immediately after the training or 30 min before the test session at the doses of 1-30 mg/kg or 3-10 mg/kg, respectively. These results suggest that caffeine differentially affects the different stages of memory processing and that this effect depends on particularities of the memory task under study.     

Tacrine treatment at high dose suppresses the recognition memory in juvenile and adult mice with attention to hepatotoxicity

It is well established that cholinergic over-stimulation can interfere with memory processes. The aim of this study was to evaluate the effect of tacrine, an acetylcholinesterase inhibitor, on recognition memory as well as the associated hepatotoxicity in juvenile (20-day-old) and adult (100-day-old) ICR male mice. Recognition memory was assessed by open-field test and step-through task without footshocks for three sessions between 08:00 and 13:00, with a 24-hr retention interval. Tacrine (10 or 40 μmol/kg) or vehicle was administered (s.c.) 20 min. prior to the first session. During the acquisition session, tacrine suppressed the open-field behaviours, including locomotor activity, rearing, grooming and defecation (by 77-100%) in mice of both ages. During the recall (observable in both ages) and re-recall (observable in juvenile mice) session, the locomotor activity and rearing number were significantly increased, indicative of impairment in recognition memory, in mice treated with tacrine 40 μmol/kg. During the training trial, tacrine decreased the step-through number in mice of both ages. In contrast, during the retention and re-retention trials, the step-through number was increased (by 92% and 93%, respectively), indicative of impairment in step-through memory, in juvenile but not adult mice treated with tacrine 40 μmol/kg. Tacrine 40 μmol/kg elevated the serum alanine aminotransferase (ALT) activity (by 135%) in juvenile mice, but reduced the ALT activity (by 42%) in adult mice. The results indicated that 20-day-old mice seemed to be more sensitive than 100-day-old mice to tacrine-induced impairment in recognition memory and the associated liver damage.     

Effects of cadmium on memory processes in mice exposed to transient cerebral oligemia

The purpose of the present study was to examine whether the effects of chronic or acute exposure to cadmium on memory processes in mice could be exacerbated by transiently reducing cerebral oxygen supply. Adult mice were subjected to bilateral clamping of the carotid artery (BCCA) for 30 min under anesthesia. Cadmium chloride was administered intraperitoneally after surgery at single doses of: 0.7 mg/kg (low dose), 1.4 mg/kg (high dose), or at a prolonged dose of 0.7 mg/kg for up to 10 days. Long-term memory was evaluated in a step-through passive avoidance task while spatial working memory was evaluated using a Y-maze spontaneous alternation task. BCCA mice injected with the 1.4 mg/kg dose of cadmium exhibited recall deficits in the step-through passive avoidance task. Combined treatment at either dose had no effect on the acquisition of passive avoidance. In the Y-maze task, spontaneous alternation behavior was only impaired in BCCA mice treated with the prolonged cadmium dose. These results indicate that cerebral oligemic hypoxia may alter cadmium neurotoxicity and potentiate the tendency for cadmium-induced memory impairments in the passive avoidance task and spontaneous alternation deficits.     

人参皂苷Rg1对β—淀粉样肽（25—35）侧脑室注射所致小鼠学习记忆障碍的改善

AIM: To study the effect of ginsenoside Rg1 on the learning and memory impairment in mice induced by aggregated beta-AP(25-35). METHODS: Mice were administered Rg1(5, 10 mg.kg-1, i.p.) for 10 d and control mice received daily i.p. injections of saline after the intracerebroventricular injection of aggregated beta-AP(25-35). After the final treatment, passive avoidance and performance in the Morris water maze (MWM) were assessed. and the activity of cortical and hippocampal ChAT and AchE were detected after the final behavior test. RESULTS: Ginsenoside Rg1 (5, 10 mg.kg-1, i.p.) significantly ameliorated the learning and memory impairment induced by beta-AP(25-35). Rg1 (5, 10 mg.kg-1) decreased the latencies and swim distances of mice to reach a hidden platform and improved the corresponding changes in search strategies occurred in the Morris water maze, and Rg1 (10 mg.kg-1, i.p.), increased step-through latencies also. Biochemical analysis showed that Rg1 (5, 10 mg.kg-1, i.p.), prevented the cortical and hippocampal ChAT activity decline induced by beta-AP(25-35), and showed inhibition of the activity of AchE, although beta-AP(25-35) showed no effect on the cortical and hippocampal AchE activity. CONCLUSION: These data showed that ginsenoside Rg1 significantly improved the learning and memory impairment induced by beta-AP(25-35), and this effect could be attributed to its inhibition of AchE and increase of ChAT activity.     

Inhibition of cerebral protein synthesis: performance at different times after passive avoidance training.

Inhibition of cerebral protein synthesis impairs long-term memory in a variety of species and tasks. Recently it was reported that subcutaneous injection of the protein synthesis inhibitor cycloheximide impaired short-term retention, measured 10 min after training in a passive avoidance task. To examine the possibility that inhibition of cerebral protein synthesis may sometimes disrupt short-term memory, mice were injected subcutaneously with cycloheximide (120 mg/kg) or anisomycin (150 mg/kg), or bitemporally with cycloheximide or anisomycin (100 mug/side) and given one training trial in a passive avoidance box. Subcutaneously injected cycloheximide reduced step-through latencies 10 min after training as reported previously, but anisomycin or bitemporally injected cycloheximide did not. All 4 drug groups exhibited impaired long-term memory. Since the results obtained at short intervals after training varied depending on the drug and route of injection, the impairment produced by subcutaneous cycloheximide at 10 min after training cannot be attributed to inhibition of cerebral protein synthesis. It is suggested that performance at short intervals after training reflects drug side effects on step-through behavior. By contrast, the impairment obtained at long intervals after training is consistent with the hypothesis that cerebral protein synthesis is required for formation of long-term memory.