镧暴露对子代大鼠学习记忆及海马组蛋白H3K4me3表达的影响

目的 探讨镧暴露对子代大鼠学习记忆能力及海马组蛋白H3赖氨酸4三甲基化（H3K4me3）水平的影响。方法 将24只SPF级雌性Wistar孕鼠随机分为对照组，2.5、5.0和10.0 g/L氯化镧（LaCl3）染毒组，其子代大鼠断乳后通过自由饮水方式按原浓度继续镧暴露。而后在不同时间采用Morris水迷宫实验检测子代大鼠的学习记忆能力，ELISA法测定海马中组蛋白甲基转移酶（HMT）的活性，Western blot法检测海马中H3K4me3和脑源性神经营养因子（BDNF）的蛋白表达水平。结果 与对照组比较，岀生后第14、21、28、35和49天LaCl3染毒组子代大鼠体质量明显下降（P<0.05）。LaCl3染毒组子代大鼠寻找逃逸平台的潜伏期延长（P<0.05），穿越平台次数和目标象限停留时间均减少（P<0.05），提示子代大鼠空间学习记忆能力受损；与对照组相比，LaCl3染毒组子代大鼠海马HMT活性降低（P<0.05），H3K4me3和BDNF蛋白表达水平均降低（P<0.05），并呈剂量-反应关系。结论 镧暴露导致子代大鼠学习记忆能力损伤可能与海马组蛋白H3K4me3表达下降有关。     

妊娠压力对大鼠子代早期空间学习记忆能力的影响

【目的】探索妊娠期精神压力对大鼠子代早期空间学习、记忆能力的影响。【方法】实验采取产前束缚压力,建立妊娠期大鼠精神压力暴露模型。然后对子代进行Morris水迷宫测试,分析妊娠期压力对子代早期学习和记忆的影响及性别间的差异,同时检测实验前、后子鼠的血清肾上腺酮的变化。【结果】①在隐蔽平台试验中,对照组的平均潜伏期较实验组短,但差异无显著性(F=0.599,P>0.05)。②在保持力试验中,对照组在原平台所在象限逗留的时间大于实验组,差异有显著性(F=4.588,P<0.05)。③子代血清肾上腺酮的测定结果表明:水迷宫测试前,实验组和对照组相比,差异无显著性(F=0.169,P>0.05);实验后,实验组血清肾上腺酮比对照组高,差异具有显著性(F=6.098,P<0.05)。【结论】①妊娠压力可导致子代学习,记忆能力的改变;②妊娠压力造成子代在应激情况下血清肾上腺酮的过度分泌。③妊娠压力对子代的影响没有明显性别差异。     

镧对大鼠海马CA3区cAMP应答元件结合蛋白磷酸化和及刻早期基因表达的影响

目的研究镧(La)对大鼠海马CA3区钙调蛋白(CaM)活性、钙调蛋白依赖性蛋白激酶IV(CaMKIV)和cAMP应答元件结合蛋白(CREB)磷酸化以及c-fos、c-jun和egr1基因表达的影响。方法 40只成年雌性大鼠随机分成对照组和低、中、高剂量LaCl3染毒组,LaCl3组仔鼠在出生至断乳前通过母乳染毒,断乳后通过自由饮水的方式染毒1个月。采用磷酸二酯酶法检测仔鼠海马CA3区CaM活性,Western blot法检测仔鼠海马CA3区p-CaMK IV和p-CREB蛋白表达水平,RT-PCR法检测仔鼠海马CA3区c-fos、c-jun和egr1mRNA表达水平。结果各LaCl3染毒组海马CA3区CaM活性和p-CaMK IV、p-CREB蛋白表达水平均显著低于对照组,且具有一定的剂量-反应关系。低、中剂量LaCl3染毒组c-fos和c-jun mRNA表达显著低于对照组,中剂量LaCl3染毒组egr1 mRNA表达显著低于对照和低剂量LaCl3染毒组,高剂量LaCl3染毒组c-fos、c-jun和egr1 mRNA表达显著低于对照和低、中剂量LaCl3染毒组。结论镧可通过降低海马CA3区CaM活性和CaMK IV、CREB磷酸化以及c-fos、c-jun和egr1基因转录水平,从而损害大鼠的学习记忆能力。     

硝酸镧对小鼠学习记忆低剂量兴奋效应及其机制研究

[目的]观察硝酸镧对小鼠学习记忆的低剂量兴奋效应及其与cAMP反应元件结合蛋白(CREB)和Jun-氨基末端激酶(JNK)蛋白磷酸化水平的关系。[方法]以0.002、0.02、0.2、2、20 mg/kg硝酸镧染毒ICR小鼠4周,每天测定小鼠水迷宫的反应时间和错误次数;试验结束时,取小鼠大脑分离海马和皮质,采用western blot测定p-CREB和p-JNK的含量。[结果]小鼠水迷宫的反应时间在染毒第4周时随着剂量的升高,呈现逐渐缩短,然后又逐渐延长的趋势,0.2 mg/kg组的反应时间最短;而错误次数则出现相反的趋势,2 mg/kg组的错误次数最少。硝酸镧经口染毒小鼠4周,0.2 mg/kg剂量组小鼠海马的CREB(6.20±3.2)和JNK(4.11±2.92)磷酸化水平升高,与溶剂对照组相比,差异有显著性。硝酸镧染毒各剂量组小鼠的皮质CREB和JNK磷酸化与对照组相比差异无显著性。[结论]硝酸镧经口染毒引起小鼠海马CREB和JNK蛋白的磷酸化水平升高,这与小鼠的学习记忆能力的变化的趋势一致,提示低剂量硝酸镧可能通过引起学习相关蛋白磷酸化水平的升高而对小鼠的空间学习记忆产生促进作用。     

镧对子代大鼠学习记忆能力、海马神经细胞钙稳态及ERK蛋白表达的影响

雌性Wistar大鼠随机分为4组,对照组饮用蒸馏水,3个染毒组分别饮用不同浓度的氯化镧(2.5 g/L,5 g/L,10 g/L)水溶液,从雌鼠受孕起至子鼠断乳后1个月连续染镧。采用Morris水迷宫检测子代大鼠学习记忆能力,Fura-2/AM探针法检测海马神经细胞内游离Ca2+浓度,Western blot法检测海马组织ERK1/2和p-ERK1/2蛋白表达水平。结果表明,随氯化镧染毒剂量的增加,子代大鼠寻找平台的潜伏期和游泳距离增加(P<0.05),在目标象限的停留时间减少(P<0.05),神经细胞内游离Ca2+水平升高(P<0.05),p-ERK1/2蛋白表达水平下降(P<0.05)。提示氯化镧染毒可以造成子代大鼠学习记忆能力下降,其原因可能与其导致神经细胞内钙稳态失衡及p-EPK1/2蛋白表达水平下降有关。 更多还原     

不同妊娠期振动对SD大鼠子代空间学习记忆的影响

目的 探讨不同妊娠期振动对大鼠子代空间学习记忆的影响。方法 分别在SD大鼠妊娠的1~7 d、8~14 d、15~21 d施加强弱交替的振动刺激,在子鼠60 d使用Barnes 迷宫测试其空间学习记忆能力,比较各组间空间学习记忆的差异。结果 学习过程:1)探索路程:妊娠早期振动组在第4天,妊娠中期在第1天,妊娠晚期在第1天高于对照组,妊娠晚期在第2、3天低于对照组(P＜0.05);2)探索平均速度:妊娠早期在第2天,妊娠中期在第1、2天,妊娠晚期在第1、2、3、7、8天均低于对照组(P＜0.05);3)错误探索时间:妊娠早期在第1、3、4、7、8天,妊娠中期在第3、4、5、8天高于对照组,妊娠晚期在第2、6天低于对照组(P＜0.05);4)首次探索目标洞潜伏期:妊娠中期在第5天高于对照组(P＜0.05)。记忆过程:妊娠早期振动组的错误探索时间明显高于对照组(Mann-Whitney U=43.00,P=0.000),妊娠晚期振动组的探索路程(Mann-Whitney U=150.00)、平均速度(Mann-Whitney U=150.00)和错误探索时间(Mann-Whitney U=164.50)明显低于对照组(P<0.05或<0.01)。结论 妊娠早期振动损害子代的空间学习记忆能力,妊娠晚期振动可能促进子代的空间学习记忆能力,而妊娠中期仅损害子代的空间学习能力。     

断乳前丰富环境对大鼠空间参考记忆及海马CA1区神经元形态学的影响

[目的]探讨断乳前丰富环境对大鼠空间参考记忆和海马CA1区锥体神经元树突结构可塑性的影响.[方法]3窝共30只新生SD大鼠,每窝均随机分为对照组(n=14)和实验组(n=16).实验组大鼠生后10日龄至24日龄每天予以丰富环境暴露20 min,对照组大鼠除不予以丰富环境暴露外,余处理均与实验组相同.生后5周,两组大鼠予以Morris水迷宫测试评估空间参考学习记忆能力.同时,采用高尔基染色法观察断乳前丰富环境对大鼠海马CA1区锥体神经元树突形态的影响,并进行统计分析. [结果]在Morris水迷宫测试中,丰富环境组大鼠的空间参考记忆成绩显著高于对照组.在训练阶段,两组到达平台的平均时间均呈下降趋势.在测试阶段,丰富环境组大鼠的空间记忆保持能力优于对照组[(31.41±5.91)%vs(26.17±5.66)%,F=4.470,P<0.05).高尔基染色显示断乳前丰富环境增加海马CA1区锥体神经元顶树突和基树突的长度[(3.46±0.65)mm vs(2.48±0.57)mm;(2.30±0.48)mm vs(1.93±0.53)mm;F=29.838,P<0.01;F=6.222;P<0.053. [结论]断乳前丰富环境可以促进大鼠空间参考记忆能力,增加海马CA1区锥体神经元顶树突和基树突的长度.     

十溴联苯醚致大鼠学习记忆及海马神经元氧化损伤和凋亡研究

目的 观察十溴联苯醚(BDE-209)对成年大鼠学习记忆及海马神经元氧化应激和凋亡的影响.方法 将96只SD雄性大鼠随机分为溶剂对照组、BDE-209低(250 mg/kg)、中(500 mg/kg)、高(1 000 mg/kg)剂量组,每天灌胃1次,持续30 d.用Morris水迷宫检测学习记忆功能,化学比色法测定大鼠海马组织总抗氧化能力(T-AOC)、谷胱甘肽转移酶( GST)、超氧化物歧化酶(SOD)、丙二醛(MDA)的水平,考马斯亮蓝法测定蛋白水平,末端标记(TUNEL)法检测海马CA1区神经元凋亡.结果 与对照组比较,BDE-209染毒组大鼠的平均逃避潜伏期明显增加、空间搜索有效策略百分比和穿越平台的次数明显减少(P＜0.05);且随染毒剂量的增加,BDE-209各组的平均逃避潜伏期明显增加、空间搜索有效策略百分比和穿越平台的次数明显减少(P＜0.05).BDE-209染毒组海马T-AOC、GST和SOD的活力明显低于对照组,MDA水平明显高于对照组(P＜0.05);并随染毒剂量的增加各染毒组T-AOC、GST和SOD的活力明显降低,MDA水平明显增加(P＜0.05).TUNEL法检测结果显示BDE-209染毒组较对照组染色深,凋亡细胞数明显增加(P＜0.05);BDE-209染毒组随染毒剂量的增加染色加深,凋亡细胞增加(P＜0.05).结论 BDE-209致成年大鼠学习记忆能力下降可能与海马神经元细胞氧化损伤和凋亡有关.     

依达拉奉改善急性一氧化碳中毒性脑病大鼠空间记忆及海马神经元凋亡的研究

目的观察自由基清除剂依达拉奉对急性一氧化碳中毒性脑病大鼠空间记忆及海马CA1区神经元凋亡的影响。方法雄性SD大鼠40只,随机均分为正常组、急性一氧化碳中毒性脑病(TE-ACMP)组、生理盐水组、依达拉奉组4组。采用Morris水迷宫检测4组SD大鼠的空间记忆,以平均逃避潜伏期衡量空间记忆能力;TUNEL法检测神经元海马CA1区神经元凋亡情况。结果 ACMP组较正常组大鼠平均逃避潜伏期明显延长(P<0.05),而依达拉奉组大鼠平均逃避潜伏期较TE-ACMP组和生理盐水组均显著缩短(P<0.05)。与正常组相比,TE-ACMP组海马CA1区凋亡指数明显升高(P<0.01)。与TE-ACMP组、生理盐水组相比,依达拉奉组海马CA1区凋亡指数明显降低(P<0.01)。结论依达拉奉可改善TE-ACMP大鼠受损的空间记忆能力,抑制TE-ACMP大鼠海马CA1区神经元凋亡,可用于临床防治一氧化碳中毒性脑病。 更多还原     

磷酸化组蛋白H3在高原地区藏族女性宫颈病变组织中的表达及意义

目的通过检测磷酸化组蛋白H3 (PHH3)在高原地区藏族女性不同级别宫颈病变组织中的表达,探讨其在宫颈病变发展中的意义。方法采用免疫组化SP法检测PHH3在144例高原地区藏族女性不同级别宫颈病变组织、不同细胞学及HPV结果中的表达情况。结果 PHH3阳性表达定位于细胞核。PHH3在宫颈组织中阳性表达情况分别为正常组织2例(7. 14%)、CINⅠ15例(50. 00%)、CINⅡ～Ⅲ23例(71. 88%)、浸润鳞癌40例(90. 91%)、浸润腺癌10例(80. 00%),各组比较差异有统计学意义(P0. 05)。在细胞学水平,PHH3的阳性表达分别为无宫颈上皮内瘤变(NILM) 28例(7. 14%)、不典型鳞状上皮细胞(ASCUS) 16例(50. 00%)、低度鳞状上皮内病变(LSIL) 32例(59. 38%)、不典型鳞状上皮不除外高度鳞状上皮内病变(ASC-H) 40例(82. 50%)、高度鳞状上皮内病变(HSIL) 28例(92. 86%),随着细胞学病变程度增加其阳性率升高,各组比较差异有统计学意义(P0. 05)。在144例宫颈病变样本中,HPV阳性患者PHH3阳性表达率高于HPV阴性患者,差异有统计学意义(P0. 05),PHH3表达水平与HPV感染呈正相关关系(r=0. 379,P0. 05)。结论 PHH3的高表达可能与高原地区藏族女性宫颈癌发生有关。     

Acute and chronic ethanol intake: Effects on spatial and non-spatial memory in rats

Abusive alcohol consumption produces neuronal damage and biochemical alterations in the mammal brain followed by cognitive disturbances. In this work rats receiving chronic and acute alcohol intake were evaluated in a spontaneous delayed non-matching to sample/position test. Chronic alcohol-treated rats had free access to an aqueous ethanol solution as the only available liquid source from the postnatal day 21 to the end of experiment (postnatal day 90). Acute alcoholic animals received an injection of 2 g/kg ethanol solution once per week. Subjects were evaluated in two tests (object recognition and spatial recognition) based on the spontaneous delayed non-matching to sample or to position paradigm using delays of 1 min, 15 min and 60 min. Results showed that chronic and acute alcohol intake impairs the rats' performance in both tests. Moreover, chronic alcohol-treated rats were more altered than acute treated animals in both tasks. Our results support the idea that chronic and acute alcohol administration during postnatal development caused widespread brain damage resulting in behavioral disturbances and learning disabilities.     

Effects of different exercise protocols on ethanol-induced spatial memory impairment in adult male rats

Chronic ethanol consumption is often accompanied by numerous cognitive deficits and may lead to long-lasting impairments in spatial learning and memory. The aim of the present study was to evaluate the therapeutic potential of regular treadmill exercise on hippocampal-dependent memory in ethanol-treated rats. Spatial memory was tested in a Morris Water Maze task. Adult male Wistar rats were exposed to ethanol (4 g/kg, 20% v/v for 4 weeks) and effects of three exercise protocols (pre-ethanol, post-ethanol and pre-to-post-ethanol treatment) were examined. Results showed that ethanol exposure resulted in longer escape latencies during the acquisition phase of the Morris Water Maze task. Moreover, all three exercise protocols significantly decreased the latency to locate the hidden platform. During the probe trial, ethanol led to decreased time spent in the target quadrant. In contrast, performance on the probe trial was significantly better in the rats that had done the post- and pre-to-post-ethanol, but not pre-ethanol, exercises. These findings suggest that treadmill running can attenuate the adverse effects of chronic ethanol exposure on spatial memory, and may serve as a non-pharmacological alcohol abuse treatment.     

Effect of acute ethanol and acute allopregnanolone on spatial memory in adolescent and adult rats

The effects of ethanol differ in adolescent and adult rats on a number of measures. The evidence of the effects of ethanol on spatial memory in adolescents and adults is equivocal. Whether adolescents are more or less sensitive to ethanol-induced impairment of spatial memory acquisition remains unclear; with regard to the effects of acute ethanol on spatial memory retrieval there is almost no research looking into any age difference. Thus, we examined the effects of acute ethanol on spatial memory in the Morris Watermaze in adolescents and adults. Allopregnanolone (ALLO) is a modulator of the GABA_A receptor and has similar behavioral effects as ethanol. We sought to also determine the effects of allopreganolone on spatial memory in adolescent and adults. Male adolescent (post natal [PN]28-30) and adult (PN70-72) rats were trained in the Morris Watermaze for 6 days and acute doses of ethanol (saline, 1.5 and 2.0 g/kg) or ALLO (vehicle, 9 and 18 mg/kg) were administered on Day 7. A probe trial followed on Day 8. As expected, there were dose effects; higher doses of both ethanol and ALLO impaired spatial memory. However, in both the ethanol and ALLO conditions adolescents and adults had similar spatial memory impairments. The current results suggest that ethanol and ALLO both impair hippocampal-dependent spatial memory regardless of age in that once learning has occurred, ethanol or ALLO does not differentially impair the retrieval of spatial memory in adolescents and adults. Given the mixed results on the effect of ethanol on cognition in adolescent rats, additional research is needed to ascertain the factors critical for the reported differential results.     

The interaction of chronic restraint stress and voluntary alcohol intake: Effects on spatial memory in male rats

Alcohol consumption and exposure to stressful life events activate similar neural pathways and thus result in several comparable physiological and behavioral effects. Alcoholics in treatment claim that life stressors are the leading cause of continued drinking or relapse. However, few studies have investigated the interactive effects of stress and alcohol on cognitive behavior. The effects of restraint stress, alcohol, and stress in combination with alcohol were examined on a spatial memory test, the object placement (OP) task. In addition, intake levels were measured to determine if stress altered general consumption of alcohol. Male Sprague-Dawley rats were assigned to one of four conditions: no alcohol/no stress control (CON), stress alone (STR), alcohol alone (ALC), and STR + alcohol (STR + ALC). Following each restraint stress bout, the STR + ALC and the ALC groups were given access to 8% alcohol for 1 h using the two-bottle choice limited access paradigm. As predicted, the STR + ALC group significantly increased alcohol consumption, while the ALC group had consistent drinking over the 10-day treatment. On the OP task, STR and ALC groups performed at chance levels, whereas the CON and STR + ALC groups significantly discriminated between objects in the new and old locations. These data show that stress increases alcohol intake and the intake of alcohol is associated with reduction of the stress-induced impairment of spatial memory. The data have important implications for the development of alcohol abuse and its treatment.     

双酚A及高脂饮食对成年大鼠空间记忆和情绪的影响

目的观察双酚A(bisphenol A,BPA)和高脂饮食(high-fat diet,HFD)慢性暴露对成年大鼠空间记忆和情绪的综合影响。方法将36只30日龄清洁级雄性Wistar大鼠随机分为4组,分别为对照(普通饲料)组、BPA(50μg/kg)组、HFD组和HFD+BPA(50μg/kg)组,每组9只。采用自由摄食方式进行染毒,连续染毒20周。分别进行Morris水迷宫试验和旷场试验。结果与对照组比较,HFD和(或)BPA组大鼠的潜伏期均延长,除第2天BPA组和第3天HFD组外,差异均有统计学意义(P0.01)。与BPA组比较,仅第2天HFD+BPA组大鼠的潜伏期延长,差异有统计学意义(P0.01)。与对照组比较,第1、2天BPA组及第3~5天HFD和(或)BPA组大鼠的游泳速度均减慢,差异均有统计学意义(P0.01)。与BPA组比较,仅第5天HFD+BPA组大鼠的游泳速度减慢,差异有统计学意义(P0.01)。与对照组相比,HFD和(或)BPA组大鼠的目标象限游泳时间和中央区停留时间均缩短,差异均有统计学意义(P0.01);而跨格子总数均无明显变化。结论双酚A和高脂饮食均可以诱发成年大鼠的空间记忆损害和焦虑行为,但其彼此无相互作用。     

Intermittent binge alcohol exposure during the periadolescent period induces spatial working memory deficits in young adult rats

Human and animal studies suggest adolescence is a period of heightened sensitivity to adverse cognitive sequelae of alcohol exposure. The present study assessed the effects of intermittent binge ethanol intoxication during the periadolescent period of Wistar rats on subsequent performance in a Morris water maze spatial navigation task. On postnatal days 32-56, rats were exposed to ethanol or air 3 days/week via vapor inhalation chambers. Acquisition of spatial navigation was assessed beginning 5 days after the final day of exposure, with 3 days of training in the Morris Water maze (four trials per day spaced at 90-s intertrial intervals [ITIs]). Rats were placed into the water maze at one of four positions along the perimeter, with a different release position to begin each trial. A probe trial assessed retention of platform location on the day after the final set of training trials. Four days after this probe trial, rats entered a working memory phase in which the platform was in a new location each day and a variable ITI of 1, 2, or 4h was inserted between Trials 1 and 2; Trials 3 and 4 followed at 90-s intervals after Trial 2 on each day. The "savings" in latency to find the platform and distance traveled before finding it from Trial 1 to Trial 2 on each day served as an index of working memory. Ethanol-exposed rats showed similar acquisition of spatial navigation as control rats during training, as well as similar retention of platform location during the probe trial. However, rats exposed to average blood alcohol level (BAL) >200mg% showed accelerated forgetting, with decreased retention of platform location at the 2-h ITI (P<.05), compared to control rats. Therefore, a 4-week history of intermittent ethanol exposure at BAL in excess of 200mg% during periadolescence led to a working memory deficit in young adult rats, demonstrated by accelerated forgetting of novel information. These behavioral data are consistent with findings from adolescent human studies, indicating that binge-style alcohol exposure during the periadolescent stage of development is associated with deficits in retention of information.     

砷对仔代大鼠神经行为和学习记忆功能影响

目的研究饮水砷暴露对大鼠仔鼠神经行为发育和学习记忆功能的影响.方法雌性大鼠于受孕后第6d开始以自由饮水方式分别暴露于10,50和100mg/L的NaAsO2水溶液,连续染毒直到仔鼠出生后第42d.观察砷对仔代大鼠生理发育、神经行为发育及学习记忆能力的影响.结果 100mg/L砷剂量组仔鼠从出生后第12d起身长、体重明显低于对照组,但张耳、开眼、长毛、出牙、抬头、爬行、站立和行走等生理发育指标与对照组相比差异无统计学意义.在神经行为测试中,100mg/L砷剂量组仔鼠尾部悬挂、听觉惊愕和视觉定位等指标阳性率显著低于对照组,出现神经行为发育迟缓.方位水迷宫实验中,各砷暴露组仔鼠在记忆获得测试和记忆保留测试中能正确寻找隐蔽平台所需训练次数显著多于对照组,说明砷对仔鼠短时记忆和长时记忆均有一定影响.结论饮水砷暴露可对仔鼠神经行为和学习记忆产生毒性作用.     

锰对大鼠空间学习记忆影响

目的探讨锰染毒大鼠空间学习记忆变化的规律。方法50只雄性大鼠适应性喂养1周后,随机分为5组,即生理盐水组(A组),Mn2+2.5,5,10,20 mg/kg(B、C、D、E组)。腹腔注射生理盐水或MnCl2溶液0.5 mL/d,共30 d。染毒结束后,采用Morris水迷宫试验测定大鼠潜伏期、总路程和穿台次数的变化。结果经多组比较的单因素方差分析,潜伏期、总路程、穿台次数各组均数间差异有统计学意义(F=7.813,P=0.000;F=8.190,P=0.000;F=3.461,P=0.000);与A组比较,B、C、D和E组潜伏期延长,差异有统计学意义(P0.05);与B组比较,D和E组潜伏期延长,差异有统计学意义(P0.05)。与A组比较,C、D和E组总路程延长,差异有统计学意义(P0.01);与B组比较,C、D和E组总路程延长,差异有统计学意义(P0.01)。与A组比较,B、C、D、E 4组穿台次数减少,差异有统计学意义(P0.05)。结论锰染毒可以引起大鼠空间学习记忆障碍。     

孕哺期高脂膳食对子代SD大鼠空间学习记忆能力的影响

目的 研究孕哺期高脂膳食对子代SD大鼠空间学习记忆能力的影响。 方法 成年雌性SD孕鼠10只随机分为对照组和高脂组,分别喂以标准鼠粮和含20%猪油的高脂饲料。仔鼠4周龄断乳,对照组雄性仔鼠10只维持原饲料,10只转饲以高脂饲料;高脂组雄性仔鼠10只维持原饲料,10只转饲以标准鼠粮。12周龄,进行Morris水迷宫测试其空间学习记忆能力,称量体重、内脏脂肪和全脑质量,测试血浆瘦素水平。 结果 持续高脂膳食的仔鼠空间学习能力低于其它仔鼠(P＜0.05),但空间记忆能力各组仔鼠无差异(P>0.05);断乳后高脂膳食可造成仔鼠体重(P＜0.05)和内脏脂肪质量(P＜0.05)增加;孕哺期高脂膳食造成仔鼠全脑质量降低(P＜0.05)和血浆瘦素水平下降(P＜0.05)。 结论 孕哺期高脂膳食造成子代脑发育障碍和血浆瘦素水平降低,这可能与子代空间学习能力损伤有关。