中国人参茎叶皂甙对大白鼠条件性行为的作用

中国人参茎叶皂甙可以提高大白鼠在MG-2型迷宫中条件性回避反应的出现率和分辨学习的正确率,并且前者的提高程度较后者更为显著。     

人参茎叶皂甙和人参根皂甙及赛庚啶对大鼠主动回避反应的影响

本文研究了人参茎叶皂甙（ＧＳＬＳ）和人参根皂甙（ＧＲＳ）及赛庚啶（ＣＹＤ）对大鼠穿梭箱主动回避反应的影响学习和记忆成绩用回避反应率（ＡＲ）和回避潜伏期（ＡＬ）评价．多次用药后，ＧＳＬＳ３０ｍｇ／ｋｇ通过显著增加ＡＲ和显著缩短ＡＬ而易化了１０月龄雄性Ｗｉｓｔａｒ种鼠单路回避反应的学习和记忆获得，但损害了雄性大鼠双路回避反应的学习获得．多次腹腔注射ＧＳＬＳ３０ｍｇ／ｋｇ和ＧＲＳ４０ｍｇ／ｋｇ均相似显著改善了由东莨菪碱（０．８ｍｇ／ｋｇ）损害的Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠单路回避反应的学习和记忆获得．此处，单次腹腔注射ＣＹＤ０．５ｍｇ／ｋｇ通过显著减少ＡＲ和显著延长ＡＬ而损害了雄性Ｗｉｓｔａｒ大鼠双路回避反应的学习的记忆获得．     

氯酯醒对正常及电休克记忆障碍大鼠学习记忆的作用

氯酯醒１５０ｍｇ／ｋｇ，１０ｄ，ｐｏ可提高大鼠训练后第７天主动性回避反应的频数（穿梭箱法）及延长大鼠训练后３ｈ，２４ｈ在台上停留时间，即被动性回避反应的潜伏期（跳台法）；使大鼠额叶、纹状体、下丘脑、海马和脑干中５－ＨＴ含量明显增加；额叶和海马ＮＡ含量明显增加；下丘脑中ＤＡ含量明显增加．氯酯醒对电休克所致的大鼠记忆障碍也表现有明显地改善作用．     

人参皂甙对慢性酒精中毒大鼠学习记忆障碍的改善作用

用50%白酒制作慢性酒精中毒大鼠模型,分别给大鼠以高、中、低剂量的人参皂甙溶液灌胃,采用三门行走迷路对实验动物的作业记忆进行测试来探讨人参皂甙对酒精慢性酒精中毒大鼠学习记忆障碍是否有改善作用,试验结果表明,人参皂甙高剂量组和人参皂武中剂量组能明显降低大鼠的错误次数,潜伏期明显降低.提示人参皂甙对慢性酒精中毒大鼠学习记忆障碍具有改善作用.     

人参皂甙对慢性酒精中毒大鼠脑组织内AchE和血清中MAO活性的影响

用50%白酒制作慢性酒精中毒大鼠模型,分别给大鼠以高、中、低剂量的人参皂甙溶液灌胃,测定大鼠脑组织内AchE和血清中MAO的活性,来探讨人参皂甙对大鼠脑组织内AchE和血清中MAO活性的影响,实验结果表明,高剂量人参皂甙能明显抑制慢性酒精中毒大鼠血清中MAO活性,提示人参皂甙对慢性酒精中毒所致的大鼠学习记忆障碍有改善作用。     

吡乙酰胺对三氯化铝中毒大白鼠回避反应受损的对抗作用

本文报道了吡乙酰胺对三氯化铝中毒大白鼠回避反应受损的治疗作用。也观察了该药对正常大白鼠回避反应的影响。结果表明吡乙酰胺加强正常大白鼠回避反应的获得(acquisition);三氯化铝抑制大白鼠回避反应的获得和保留(retention),吡乙酰胺有对抗作用。     

丁基苯酞对局部脑缺血大鼠记忆障碍的影响

观察了丁基苯酞（ＮＢＰ）对局部脑缺血大鼠记忆障碍的影响．用穿梭箱进行学习记忆获得性训练，以主动回避反应潜伏期和次数以及逃避反应潜伏期为指标，评价大脑中动脉阻断（ＭＣＡＯ）后记忆保持的能力．结果表明：假手术组的记忆功能与正常组没有显著差别，而缺血对照组大鼠主动回避反应次数减少６０％，主动回避和逃避反应潜伏期分别较缺血前延长４．２±１．６和４．１±３．３ｓ．给ＮＢＰ３０和１００ｍｇｋｇ－１后主动回避反应的次数明显提高，主动回避反应潜伏期明显缩短，与缺血对照组比较均有非常明显的差别．表明ＮＢＰ对局部脑缺血引起的记忆障碍有明显改善作用．     

小鼠暂时性脑缺血引起学习记忆障碍模型的制备及人参皂甙的保护作用

人参皂甙是人参的主要有效成分。本文在建立小鼠脑缺血再灌注导致学习记忆障碍模型的基础上，用跳台、避暗两种实验方法观察了人参皂甙对小鼠脑缺血再灌注后学习记忆功能的保护作用。结果显示小鼠脑缺血再灌注可以导致学习记忆障碍，而人参皂甙（１０，１００ｍｇ·ｋｇ－１，ｐｏ）可以对这种记忆障碍起到保护作用。     

依据自由基学说研究人参茎叶皂甙的抗衰老作用

本文从衰老的自由基损伤学说出发研究了人参茎叶皂甙的抗衰老作用。结果表明,人参茎叶皂甙能显著地抑制小鼠脑、肝组织中的脂质过氧化,提高红细胞中超氧化物歧化酶含量和过氧化氢酶活性,并对大鼠大脑皮质和肝脏中脂褐素生成有显著的抑制作用.提示人参茎叶皂甙具有较强的抗氧化作用,并可能具有抗衰老活性。     

人参二醇皂甙对沙土鼠急性脑缺血－再灌注损伤的保护作用

人参二醇皂甙对沙土鼠急性脑缺血－再灌注损伤的保护作用王国贤宗瑞义１刘丹平２（锦州医学院药理教研室，锦州１２１００１）中国图书分类号Ｒ９７１；Ｒ９３１．７；Ｒ２８４．１人参二醇皂甙（ＰａｎａｘａｉｏｌＳａｐｏｎｉｎ，ＰＤＳ）是从吉林人参茎叶中分离出来的...     

Piracetam and fipexide prevent PTZ-kindling-provoked amnesia in rats

Deficit in active and inhibitory avoidance behaviour has been found in pentylenetetrazole (PTZ)-kindled rats. This supports the view that memory deficit is an integral part of epilepsy. In the present study we examined the effect of the nootropic drugs piracetam and fipexide on memory deficit induced by PTZ-kindling in shuttle-box- and step-down-trained rats. The retention in piracetam- and fipexide-treated animals was significantly improved compared to the kindled controls. The mechanisms of action of the two drugs are considered. The favourable effects of nootropic drugs in cases of amnesia provoked by PTZ-kindling might be of interest in clinical practice.     

Dihydroergocristine and memory alterations of aged male rats

The ergot alkaloid derivative dihydroergocristine (DHECS) was injected acutely or subchronically to aged male rats of the Sprague-Dawley strain, 26 months old, at the dose of 0.05 or 0.1 mg/kg. Learning and memory ability of the animals were studied with tests of avoidance behavior. The acquisition of active avoidance behaviour was also studied. A step-throug type of passive avoidance task In the latt, the extinction of active avoidance behavior was also studied. A step-through type of passive avoidance task was used to examine the retention of passive avoidance responses. The acquisition of the active avoidance behavior and the retention of the passive avoidance response were reduced in aged animals as animals as compared to those of young animals. Acute treatment of old rats with DHECS was followed by a facilitation of acquisition of active avoidance behavior in the shuttle box and of retention of passive avoidance responses in the dark box. The effect on the acquisition and extinction of pole-jumping behavior after a single injection of DHECS at the beginning of the acquisition session was restricted tot he first acquisition trial. A more potent effect on the acquisition of the shuttle-box behavior and on the retention of passive avoidance reaction was found in animals treated subchronically with the ergot derivative (0.05 and 0.1 mg/kg for 10 days). These rats also showed a facilitation of acquisition and an inhibition of extinction of pole jumping behavior.     

Learning ability in adult female rats perinatally exposed to methadone

Cognitive functioning of adult female rats that were maternally exposed to methadone (5 mg/kg daily) during gestation and/or lactation was studied by assessing performance on a food-motivated light-dark discrimination learning test and on active and passive shock-avoidance tests. Methadone-exposed rats exhibited difficulties on the light-dark discrimination learning and the active avoidance tests, and behavioral deficits appeared to be related to the timing and duration of drug treatment. On the light-dark discrimination test only 33% of the rats in the gestation group and 25% of the animals in the lactation group met criterion in comparison to 87% of the control rats. Thirty-three percent of the animals in either the gestation or gestation-lactation groups met criterion on the active avoidance test in contrast to 87% of the controls. These data suggest that perinatal exposure to methadone impairs cognitive abilities in the adult female rat.     

Residual effects of prolonged cannabis treatment on shuttle-box avoidance in the rat

Chronic oral administration of cannabis extract to rats was examined for its residual effects on shuttle-box avoidance learning. In experiment 1 avoidance learning was assessed in rats that had been tested previosly on other behavioral tests. Chronic treatment (3 months) facilitated the learning of shuttle-box avoidance in cannabis-treated animals relative to vehicle controls. In experiment 2 very similar results were obtained in naive rats. These and other residual effects of chronic cannabis treatment are similar to the effects of hippocampal lesions.     

Learning and Memory of Rats after Long-Term Administration of Low Doses of Parathion

A set of four learning and memory tests (Morris Maze I for referencememory, Morris Maze II for working memory, one-way active avoidance,and passive avoidance) were employed to address the questionswhether parathion impaired cognitive functions after low, long-termexposure and could cause persistent changes in cognition. Motoractivity and general behavior were investigated in a functionalobservational battery. Parathion was administered in rat foodin low doses which caused no clinical symptoms and no or borderlinebrain acetylcholinesterase inhibition. Parathion doses of 0.5,2, or 8 ppm in rat food produced the averaged uptake of 24,100, or 400 µg/kg body weight per group per day in malerats and 36, 152, or 550 µg/kg per day in female ratsin week 13. Learning tests were performed in weeks 1 to 4 and10 to 14, as well as 30 to 34 weeks after the end of treatment,when the male and female rats were about 13 months old. Lowdoses of parathion given daily for 13 weeks had no cumulativeor adverse effects on learning and memory, either during treatmentor after the extended treatment-free period, in any of the tests.A significant improvement of learning compared to control observedin the Morris Water Maze I during the first week of treatment(males dose group 0.5 ppm) shows that parathion can improvedcognitive functions in rats. Results of the study indicate thatadverse effects changing learning and memory in animals mayoccur only at higher doses of organophosphates, at which theperipheral and brain acetylcholinesterases are inhibited toa greater extent than those in the present Study.     

Effects of different doses of glucose and insulin on morphine state-dependent memory of passive avoidance in mice

Rationale Behavioral effects of morphine, including its effect on memory, have been demonstrated to be influenced by glucose pretreatment. The measurement of step-down latency in passive avoidance has been used to study memory in laboratory animals. The pre-training injection of 5 mg/kg morphine impaired memory, which was restored when 24 h later the same dose of the drug was administered.Objectives To investigate the effects of glucose and insulin alone or in combination with morphine, on pre-test day, on memory recall in mice.Methods The effects of different doses of glucose (50, 100, and 200 mg/kg, IP) and insulin (5, 10, and 20 IU/kg, IP) alone or in combination with morphine, have been studied in mice. The blood glucose level and locomotor activity of the animals were also measured.Results Although the administration of glucose alone showed no effect on morphine-induced memory impairment, its co-administration with morphine resulted in a significant and dose-dependent memory enhancement compared with the effects of morphine administration alone. Like glucose, the administration of different doses of insulin alone produced no change in the memory, but when the drug was co-administered with morphine, it significantly reduced morphine-induced memory retrieval. The effect of insulin was the opposite of glucose. None of the animals subjected to insulin treatment showed convulsions.Conclusions Glucose is suggested to increase, on the test day, the morphine-induced memory enhancement by three different mechanisms: cholinergic or opioidergic modulations, or regulation of the ATP-dependent potassium channels.     

Differential effects of anxiogenic central and peripheral benzodiazepine receptor ligands in tests of learning and memory

Previous research has demonstrated that low doses of anxiogenic central benzodiazepine receptor (CBR) ligands, the beta-carbolines, improve performance in various learning and memory tests in animals if administered prior to training. The present experiments compared the effect of a beta-carboline (FG 7142) with that of a pharmacologically distinct anxiogenic compound, a peripheral benzodiazepine receptor (PBR) ligand, 4-chlorodiazepam (Ro5-4864), in two tests of learning and memory in rats. As expected, FG 7142 significantly improved performance in a passive avoidance test. Ro5-4864 was without effect. In a shuttlebox escape test, Ro5-4864 significantly impaired performance while FG 7142 had no effect. The effect of Ro5-4864 was antagonized by the specific peripheral benzodiazepine receptor antagonist, PK 11195. These results indicate that the differential impact of CBR and PBR anxiogenic ligands on performance in aversively-motivated learning tests may be a reflection of their distinct pharmacologies.     

十二种化学药品破坏小鼠被动回避性行为——跳台试验和避暗试验的作用的比较观察

采用小鼠一次性学习行为——跳台和避暗反应法,观察了十二种化学药品对学习和记忆获得,巩固和再现的影响,结果表明,M-胆碱能拮抗剂、儿茶酚胺耗竭剂和多巴胺拮抗剂可破坏记忆的获得;中枢抑制剂可破坏记忆的获得和/或记忆的再现;除三尖杉酯碱的其它两种蛋白质生物合成抑制剂和RNA生物合成抑制剂可破坏记忆的巩固。上述大多数化学药品虽可在两种试验方法中得到相似的结果,但对记忆获得和记忆巩固的损害,跳台法较避暗法更敏感。以上两法均系值得采用的简易快速的学习记忆试验。     

Reversal of cycloheximide-induced memory disruption by AIT-082 (Neotrofin) is modulated by,but not dependent on,adrenal hormones

Rationale. AIT-082 (Neotrofin), a hypoxanthine derivative, has been shown to improve memory in both animals and humans. In animals, adrenal hormones modulate the efficacy of many memory-enhancing compounds, including piracetam and tacrine (Cognex). Objective. To investigate the role of adrenal hormones in the memory-enhancing action of AIT-082. Methods. Plasma levels of adrenal hormones (corticosterone and aldosterone) in mice were significantly reduced by surgical or chemical (aminoglutethimide) adrenalectomy or significantly elevated by oral administration of corticosterone. The effects of these hormone level manipulations on the memory-enhancing activity of AIT-082 and piracetam were evaluated using a cycloheximide-induced amnesia/passive avoidance model. Results. As previously reported by others, the memory enhancing action of piracetam was abolished by adrenalectomy. In contrast, the memory enhancement by 60 mg/kg AIT-082 (IP) was unaffected. However, a sub-threshold dose of AIT-082 (0.1 mg/kg, IP) that did not improve memory in control animals did improve memory in adrenalectomized animals. These data suggested that, similar to piracetam and tacrine, the memory enhancing action of AIT-082 might be inhibited by high levels of adrenal hormones. As expected, corticosterone (30 and 100 mg/kg) inhibited the action of piracetam, however no dose up to 100 mg/kg corticosterone inhibited the activity of AIT-082. Conclusions. These data suggest that while AIT-082 function is not dependent on adrenal hormones, it is modulated by them. That memory enhancement by AIT-082 was not inhibited by high plasma corticosterone levels may have positive implications for its clinical utility, given that many Alzheimer's disease patients have elevated plasma cortisol levels. Electronic Publication     

Beneficial effects of ellagic acid against animal models of scopolamine- and diazepam-induced cognitive impairments

Context In a previous study, it has been shown that ellagic acid (EA), a polyphenolic compound found in pomegranate and different berries, prevents cognitive and hippocampal long-term potentiation (LTP) impairments induced by traumatic brain injury in rats through antioxidant and anti-inflammatory mechanisms.

Objective The present study was conducted to assess the potential of EA as a memory enhancer.

Materials and methods The elevated plus maze (EPM) and passive avoidance (PA) paradigm were used to evaluate learning and memory parameters. Three doses (10, 30 and 100?mg/kg, i.p.) of EA were administered to animals. Memory impairment was induced by scopolamine treatment (0.4?mg/kg, i.p.) and/or diazepam (1?mg/kg, i.p.). Acquisition trials were carried out 30?min after scopolamine treatment and retention trials were performed for 5?min 24?h after the acquisition trials.

Results EA at doses 30 and 100?mg/kg significantly reversed the amnesia induced by scopolamine (0.4?mg/kg, i.p.) in the EPM and PA tests in mice. Also, EA at doses 30 and 100?mg/kg significantly antagonized the amnesia induced by diazepam (1?mg/kg, i.p.) in EPM test in rats. Moreover, chronic administration of EA at dose 30?mg/kg ameliorated the memory deficit induced by diazepam (1?mg/kg, i.p.) in rats.

Discussion and conclusion This study demonstrates that ellagic acid is effective in preventing scopolamine- and diazepam-induced cognitive impairments without altering the animals’ locomotion. This suggests the potential of EA application as a useful memory restorative agent in the treatment of dementia seen in elderly persons.