应用程序控制行为测试研究甲基汞和微波对仔鼠神经行为的影响

[目的]应用程序控制行为测试分别评价妊娠期暴露于氯化甲基汞、频率1800MHz低强度微波辐射对F1 代大鼠的神经行为毒性。[方法]Wistar大鼠以雌雄2∶1合笼交配 ,受孕母鼠随机分组。实验1:于孕鼠妊娠第6～9d给予氯化甲基汞 ,0、0.01、0.05、2.00mg/(kg·day)连续灌胃染毒。随机选择32只F1 代大鼠 (雌雄各半 )于10周龄时进行程序控制行为测试。实验2:于孕鼠妊娠第1～20d暴露于频率为1800MHz,功率密度为0.5、1.0mW/cm2 的微波辐射 ,对照组为虚拟暴露 ;随机选择48只F1 代大鼠 (雌雄各半 )于10周龄时进行程序控制行为测试。[结果]实验1:甲基汞3个剂量组大鼠的学习成绩在两种程序均比对照组降低 (P<0.05或P<0.01) ,存在剂量_反应关系 (高频度差别强化率rs= -0.7273 ,P<0.01;低频度差别强化率rs= -0.2238,P>0.05)。实验2:1800MHz、功率0.5mW/cm2 微波组雄性仔鼠在高频度差别强化率 (DRH8/4)的成绩比对照组降低 (P<0.05)。[结论]胚胎期暴露于低剂量甲基汞对大鼠可产生神经行为毒性 ,表现为学习记忆功能异常 ;出生前暴露于频率1800MHz微波对仔鼠神经行为发育的影响尚不能确定。     

胚胎期低剂量甲基汞暴露大鼠的操作行为测试

目的 建立起电脑控制的大鼠操作行为测试系统,探讨胚胎期低剂量甲基汞暴露对大鼠学习记忆能力的影响。方法 以氯化甲基汞0,0．01,0．05,2．00mg(kg.d)于Wistar孕鼠妊娠6－9d进行灌胃处理。仔鼠10周龄时,于4个实验组中各随机抽取8只,采用自动化操作行为测试系统于夜间进行15h（16：00－7：00）的行为测试,测试程序为高／低频度差别强化率,前者要求大鼠多次重复压杆,后者则需要在得到强化物（45mg小食丸）后等待一段时间再压杆。实验采用双盲法。结果 3个剂量组大鼠的学习成绩均比对照组降低（P＜0．05或P＜0．01）,高频度差别强化率存在剂量－反应关系（rs＝－0．7273,P＜0．01）。结论 胚胎期低剂量甲基汞暴露可影响大鼠神经系统的生长发育,使其学习记忆能力受到损伤。     

甲基汞对亲仔两代大鼠的神经行为毒性效应

目的探讨大鼠妊娠期甲基汞暴露的母体毒性及对仔代的神经行为毒性效应。方法Wistar孕鼠52只于妊娠第6～9天用甲基汞0.00、0.01、0.05、2.00mg/(kg·d)连续灌胃。分别观察母体毒性 ;常规致畸实验 ;记录205只仔鼠早期生理发育和神经行为发育指标 ;10周龄仔鼠32只进行程序控制行为测试 ;分娩后5周母鼠和10周龄仔鼠各24只进行脑组织形态学观察和单胺类神经递质的测定。实验遵循随机、双盲原则。结果未观察到母体毒性和仔代形态畸形 ;3个暴露组胎仔的体重、尾长低于对照组 (P<0.01) ;各暴露组仔鼠体重增长、早期生理及神经行为发育滞后于对照组 (P<0.05) ;程序控制行为学习成绩比对照组降低 (P<0.05) ,有剂量_效应关系 (rs= -0.7273 ,P<0.01) ;各暴露组母鼠和仔鼠脑组织无形态学改变 ,但单胺类神经递质含量均比对照组显著增高 (P<0.05) ,有剂量_效应关系 (rs=0.7124～0.9257 ,P<0.01)。结论本研究剂量的妊娠期甲基汞暴露未观察到对孕鼠的毒性效应 ,但有轻度胚胎毒性 ,影响仔鼠的神经系统发育 ,导致仔鼠学习记忆能力降低 ,亲仔两代大鼠脑组织中单胺类神经递质的含量增高     

胚胎期暴露于甲基汞大鼠的迷宫测试

为研究胚胎期甲基汞暴露对大鼠迷宫学习与记忆能力的影响 ,用不同剂量甲基汞 [0、0 .0 1、0 .0 5和 2 .0 0 mg/ (kg· d) ]于大鼠孕 6～ 9天连续灌胃染毒 ,仔鼠出生 7周时进行 Y型迷宫测试。学习记忆成绩以平均错误次数、到达安全区平均时间和主动回避率表示。整个实验采用双盲法。结果与对照组相比 ,各暴露组大鼠的平均错误次数和到达安全区平均时间显著增高 ,主动回避率显著降低 (P<0 .0 5或 P<0 .0 1) ;各组大鼠学习记忆能力无性别差异。提示甲基汞可通过胎盘屏障和乳汁进入仔鼠体内 ,影响仔鼠神经系统的发育 ,使其学习记忆能力受到明显损害     

母体铅暴露对仔鼠学习和记忆的持续性效应研究

为研究母体铅暴露对大鼠子代学习和记忆发育的持续性效应 ,将孕鼠随机分为 4组 ,从孕期第 1天至仔鼠出生第 2 0天断乳分别饮用双蒸水、2 0 0、10 0和 5 0mg L醋酸铅溶液。水迷宫测试 2 0天龄仔鼠学习能力 ;Y迷宫测试 2 0天龄、40天龄、60天龄仔鼠主动学习和记忆能力。结果显示 ,(1)仔鼠水迷宫错误次数随母鼠铅暴露剂量增加而增加 ,中、高剂量组明显低于对照组 ;其逃避潜伏期则不明显 ,只有高剂量组低于对照组。 (2 )各剂量组仔鼠Y迷宫 0min、10min、2 4h逃避达标率 2 0天龄时最低 ,停止染毒 2 0、40天后虽有所恢复 ,但与对照组相比仍有显著性差异。结论 :(1)母体铅暴露先损伤仔鼠的学习和记忆能力 ,其次损伤运动能力。 (2 )母体铅暴露可损伤仔鼠的空间学习和记忆能力 ,停止染毒后虽有一定恢复但损伤仍然存在     

邻苯二甲酸丁苄酯对大鼠神经行为发育的影响

目的 研究邻苯二甲酸丁苄酯(BBP)对Wistar大鼠早期行为和学习记忆等神经行为发育的影响.方法 4周龄健康雌性大鼠80只,随机分为对照组和3个剂量染毒组,分别喂饲含0、0.05%、0.25%、0.75%BBP的饲料至F1代仔鼠6周龄.F0代雌鼠性成熟后与健康成年雄鼠交配,F1代仔鼠断乳后染毒剂量和方式与F0代雌鼠一致.染毒时间包括F0代雌鼠交配期、孕期及哺乳期,以及F1代仔鼠的生长发育期.观察F1代仔鼠的生长发育及神经行为状态.结果 (1)F1代雄鼠:4日龄仔鼠平面翻正试验:中剂量组的评分(56分)低于对照组(61分),差异有统计学意义(P＜0.05);7日龄仔鼠悬崖回避试验:高剂量组评分(41分)低于对照组,差异有统计学意义(P＜0.05);14日龄仔鼠空中翻正试验:各染毒组的翻正率均低于对照组,差异有统计学意义(P＜0.05);开阔场试验:低剂量组和高剂量组雄性仔鼠穿行格子数均大于对照组,差异有统计学意义(P＜0.05);水迷宫试验:第5天的定位航行实验中,低剂量组雄性仔鼠的平均潜伏期比对照组明显延长,差异有统计学意义(P＜0.05).(2)F1代雌鼠:各组早期行为发育指标和开阔场试验结果与对照组比较,差异均无统计学意义(P＞0.05).结论 BBP可能只对F1代雄性大鼠的早期行为和神经行为发育产生一定的影响.     

孕哺期大鼠全氟辛烷磺酸暴露对子代糖代谢的影响

[目的]探讨孕哺期全氟辛烷磺酸(PFOS)暴露对子代大鼠糖代谢的影响. [方法]将Wistar孕鼠自孕0天(GD0)随机分为对照组(0mg/kg)、低剂量组(0.6 mg/kg)和高剂量组(2mg/kg),每组10只;PFOS灌胃染毒至仔鼠出生后21天(PND21)断乳为止.采用高效液相/质谱法检测PND0、PND21时仔鼠血清PFOS含量;观察仔鼠体重变化趋势;比较9周龄和15周龄仔鼠空腹血糖、空腹胰岛素水平;检测仔鼠瘦素和抵抗素基因表达水平变化. [结果] PND21时低剂量组和高剂量组仔鼠血清中PFOS浓度分别为(16.00±1.27)mg/L和(80.54±6.55) mg/L(P＜0.05).低剂量组雌性仔鼠出生后8、9周龄和高剂量7～9周龄,低剂量组雄性仔鼠出生8～12周龄、高剂量7、8、10周龄的体重均明显低于对照组(均P＜ 0.05).高剂量组9周龄和低剂量组15周龄雌性仔鼠的胰岛素水平分别为(10.85±1.37)mU/L和(13.62±1.87) mU/L,均高于对照组(P＜0.05);高剂量组9周龄雄性仔鼠的空腹血糖和胰岛素水平分别为(5.43±0.77) mmol/L和(13.23±1.81)mU/L,15周龄雄性仔鼠低剂量组分别为(4.99±0.54) mmol/L和(13.57±1.22)mU/L,15周龄高剂量组分别为(5.71±0.56) mmol/L和(13.44±2.97)mU/L,均高于对照组(P＜0.05).高剂量组15周龄雄性仔鼠的抵抗素基因表达上调1.25±0.03(P＜ 0.05),瘦素基因表达下调0.67±0.08(P＜0.05). [结论]PFOS孕哺期暴露可能引起子代大鼠糖代谢异常,增加糖尿病患病风险.     

母鼠低剂量接触甲基汞所致仔鼠学习能力及脑海马超微结构的变化

[目的]研究ICR母鼠饮水暴露低剂量氯化甲基汞(MeHgCl)后,仔鼠脑组织的病理组织学变化和脑海马超微结构变化,评价低剂量饮水暴露甲基汞的安全性。[方法]ICR孕鼠随机分为对照组、低剂量组和高剂量组,每组各8只,各组于怀孕第6天起,分别自由饮用蒸馏水和氯化甲基汞含量为0.01、0.1mg/L的蒸馏水,直至哺乳期结束。测试各组仔鼠学习能力,观察仔鼠脑组织病理组织学变化及脑海马超微结构变化。[结果]在对仔鼠进行学习能力测试的水迷宫实验中,对照组、低剂量组和高剂量组成功率分别为81.67%、59.09%和70.00%,低剂量组和高剂量组成功率显著低于对照组(P<0.05)。低剂量组和高剂量组仔鼠脑组织有明显的病理学改变,随着甲基汞染毒剂量的增加,海马区大锥体细胞、大脑神经元和小脑浦肯野细胞嗜酸性增强。电镜结果显示,低剂量和高剂量组脑海马神经细胞有变性,严重者呈暗细胞表现。[结论]实验剂量甲基汞可使仔鼠脑组织发生病理组织学改变,脑海马区超微结构改变,实验剂量甲基汞对于仔代是不安全的。     

甲基汞对幼年大鼠认知及甲状腺激素的干扰效应

目的探讨出生后早期暴露甲基汞(MMC)所致仔鼠神经行为的发育毒性及对甲状腺激素的干扰作用。方法将112只新生清洁级大鼠随机分为对照组(生理盐水)和低(0.5mg/kg)、中(1.0mg/kg)和高(2.0mg/kg)剂量MMC染毒组,每组28只。于出生后第2～8天,采用口服方式进行染毒,染毒容量为1.0ml/kg。评价仔鼠一般生理指标和反射行为发育,采用恋窝实验和水迷宫实验检测感官、认知和记忆,并检测血中游离甲状腺激素(T4)、三碘甲腺原氨酸(T3)含量和促甲状激素(TSH)活性。结果与对照组相比,MMC染毒仔鼠的生长发育及一般神经行为发育基本无变化。在恋窝实验中,随着MMC染毒剂量的升高,仔鼠达标率呈下降趋势,达标仔鼠潜伏时间呈延长趋势。在传统水迷宫实验中,MMC染毒仔鼠游泳时间缩短;在反向水迷宫实验中,MMC染毒仔鼠游泳时间延长。与对照组比较,高剂量MMC染毒组仔鼠全血中游离T4含量较高,T3含量较低,而MMC染毒组仔鼠全血中TSH活性均较高,差异有统计学意义(P0.05或P0.01)。结论出生后早期MMC暴露可明显影响仔鼠的感觉、学习和认知能力,其机制可能与甲状腺激素紊乱有关。     

出生前暴露甲基对硫磷与氯氰菊酯混配农药对大鼠子代神经行为毒性的影响

[目的]探讨出生前甲基对硫磷与氯氰菊酯混配染毒,对大鼠子代神经行为发育的影响. [方法]48只Wistar孕鼠随机分为4组,于妊娠第1～15天用农药甲基对硫磷与氯氰菊酯进行连续灌胃染毒,对照组采用溶剂灌胃.甲基对硫磷剂量分别为:0,0.0230,0.0725,0.2300mg/kg体重;氯氰菊酯剂量分别为0,0.8000,2.5265,8.0000mg/kg体重.甲基对硫磷与氯氰菊酯采用等毒性混配,即分别为:0、1/300 LD50、1/95 LD501/30LD250,对349只仔鼠进行早期神经行为发育指标的测试;对64只仔鼠进行Morris水迷宫空间学习和记忆能力的测试. [结果]仔鼠断崖回避达标率在出生的第5、6天,高、中剂量组低于对照组(P＜0.05);视觉定位达标率在出生的第16天下午,高、低剂量组低于对照组(P＜0.05) Morris水迷宫实验测试指标,各剂量组与对照组差别无显著性(P＞0.05). [结论]大鼠孕期暴露于甲基对硫磷与氯氰菊酯混配农药,对仔鼠的神经行为发育可产生一定的影响.     

Maternal supplementation with a complex milk lipid mixture during pregnancy and lactation alters neonatal brain lipid composition but lacks effect on cognitive function in rats

Complex milk lipids (CMLs) provide a critical nutritional source for generating both energy and essential nutrients for the growth of the newborn. The present study investigated nutritional supplementation with a CML containing gangliosides and phospholipids in pregnant and lactating rats on learning behavior and postnatal growth in male offspring. Wistar female rats were supplemented during pregnancy and lactation with either control or CML to provide gangliosides at a dose of 0.01% (low) and 0.05% (high) based on total food intake. The CML-supplemented dams showed no differences in comparison to controls regarding growth, food intake, and litter characteristics. There were significant differences in brain composition in male offspring at postnatal day 2 (P2) with higher concentrations of gangliosides (high dose, P < .05) and lower concentrations of phospholipids (low and high dose, P < .05) in the CML-supplemented groups. The distribution of individual ganglioside species was not significantly different between treatment groups. Brain weight at P2 was also significantly higher in the CML groups. Differences in the brain composition and weight were not significant by weaning (P21). As adults (P80), adiposity was reduced in the low CML-supplemented group compared to controls. No significant differences were detected between any of the treatment groups in any of the behavioral tasks (water maze, object recognition, and operant learning). These data suggest that maternal supplementation with a CML during pregnancy and lactation is safe and has a significant early impact on brain weight and ganglioside and phospholipid content in offspring but did not alter long-term behavioral function using standard behavioral techniques.     

孕期暴露苯并[a]芘对子代大鼠神经发育毒性的影响

目的 研究孕期暴露苯并(a)芘(B[a]P)对子代大鼠生理发育、早期行为发育、对环境的适应能力及学习记忆能力的影响.方法 SD孕鼠随机分为未处理对照组(每日正常饲养)、溶剂对照组(橄榄油)、低剂量组(25mg/kgB[a]P)、中剂量组(50mg/kgB[a]P)、高剂量组(100mg/kg B[a]P),于妊娠第17天开始,每天1次腹腔注射染毒,连续3 d,待其自然分娩.仔鼠出生后第1、4、7、14、28天称量体重,检测仔鼠生理发育、运动反射及感觉功能等发育指标,用Morris水迷宫试验和旷场试验分别评价仔鼠的学习记忆能力和对新异环境的适应能力.结果 与未处理对照组[(3.3±0.5)d]和溶剂对照组[(3.4±0.6)d]比较,中、高剂量组仔鼠张耳时间[(4.1±0.4)、(5.0±0.4)d]延长,差异有统计学意义(P＜0.01).与未处理对照组(36、1%)相比,第4天高剂量组平面翻正试验达标率(6.5%)明显降低,与未处理对照组和溶剂对照组(81.3%、79.3%)相比,第7天时高剂量组仔鼠平面翻正试验达标率(50.0%)明显降低,差异有统计学意义(P＜0.05).与未处理对照组比较,第12、14天时各染毒组仔鼠前肢悬挂时间均减少;与溶剂对照组比较,第14天时高剂量组仔鼠前肢悬挂时间减少,差异有统计学意义(P＜0.01).与未处理对照组(94.3%)相比,第12天时高剂量组仔鼠嗅觉定向试验达标率(61.9%)明显降低,差异有统计学意义(P＜0.05).Morris水迷宫试验结果表明,与未处理对照组和溶剂对照组比较,各剂量组仔鼠逃避潜伏期明显增加,高剂量组在目标象限停留时间和穿越平台次数减少,差异均有统计学意义(P＜0.01).旷场实验结果表明,与未处理对照组[(2.40±0.89)、(82.2±15.9)、(17.4±3.9)s]比较,中、高剂量组仔鼠中央格停留时间[(9.67±1.53)、(12.80±3.77)s]明显延长,跨格次数(51.3±8.7、49.4±20.0)明显减少,高剂量组直立次数(8.0±2.6)明显减少,差异均有统计学意义(P＜0.05);与溶剂对照组相比,各剂量组跨格次数明显减少,差异均有统计学意义(P＜0.01,P＜0.05).结论 孕期暴露B[a]P对仔鼠的生理发育、早期行为发育产生一定的抑制作用,并对仔鼠大脑学习记忆能力及其对新异环境的适应能力有一定影响.

Abstract：

Objective To study the effects of prenatal exposure to benzo[a]pyrene (B[a]P) on the physical development, early behavioral development, the adaptability to new environment and the learning and memory ability of rat offspring. Methods Pregnant rats were randomly divided into five groups: control group,olive oil group, 3 exposure groups (25, 50 and 100 mg/kg B [a]P). The rats were exposed to B [a]P) by intraperitoneal injection on the 17th-19th days during gestation. The offspring were weighed on postnatal days (PND)1, PND 4, PND 7 and PND 28, the indices of physical development, reflective ability and sensory function were detected for offspring, the Morris water maze and Open-field tests were used to measure the ability of learning and memory and the adaptability to new environment of offspring. Results The time of ear opening in middle and high-dose groups[(4. 1 ±0.4),(5.0±0.4) d] was posterior to that in untreated and solvent groups[(3.3±0.5),(3.4±0.6) d](P＜0.01).The attainment rate (6.5%) of the surface righting reflex test in highdose group on the 4th day was significantly lower than that (36.1%) in untreated group, the attainment rate(50.0%) in high-dose group on PND7 was significantly lower than those (81.3% and 79.3%) in untreated group and solvent group (P＜0.05). Compared to the untreated group, the time of forelimb hanging test in all exposure groups on PND12 and PND14 significantly decreased; compared to the solvent group the time of forelimb hanging test decreased in high-dose group on the 14th day significantly decreased (P＜0.01). The attainment rate (61.9%) of olfactory discrimination in high-dose group on PND 12 was significantly lower than that (94.3%) in untreated group (P＜0.05). The results of morris water maze test showed that the escape latency of different dose groups significantly increased, and the time of spatial probe and the times of traversing flat in high-dose group decreased significantly, as compared to the untreated and solvent groups(P＜0.01). The results of open-field test indicated that the center retention time in middle and high-dose groups significantly prolonged, the times of crossing lattice obviously reduced, and the rearing times decreased in high-dose group,as compared to untreated(P＜0.05).Compared to the solvent group, the times of crossing lattice in all exposure groups reduced significantly(P＜0.01 or P＜0.05). Conclusion The prenatal exposure to B[a]P could inhibit the physical development and early behavioral development, and influence the adaptability to new environment and learning and memory ability for offspring.     

慢性染汞大鼠皮质胆囊收缩素神经元的变化

目的:观察染汞大鼠皮层内CCK阳性神经元的变化与大鼠学习记忆能力之间的关系。方法:选用刚断乳健康Wistar大鼠16只,雄性,由天津市实验动物中心提供。随机分为两组,每组8只,即对照组(饮用单蒸水,普通饲料)、染汞组(饮用4.3 mg/(kg.d)氯化汞水,普通饲料),1月后进行实验。采用Y迷宫方法观察染汞大鼠在学习记忆方面与对照组大鼠的差别。采用CCK抗体免疫组化方法,观察饮用含4.3 mg/(kg.d)氯化汞(HgCl2)饮水的大鼠皮层CCK阳性神经元的变化。结果:染汞大鼠较对照组大鼠学习记忆能力明显降低,差别有显著性;染汞组大鼠皮层CCK阳性神经元的数量较对照组明显减少,差异有显著性。结论:染汞后大鼠皮层CCK阳性神经元表达的减少,可能是汞影响学习记忆的机制之一。     

母体铅暴露对大鼠子代学习和记忆的影响

目的 研究母体铅暴露对大鼠子代学习和记忆的影响。方法 孕鼠随机分为4组,从孕期第1天至仔鼠出生第20天断乳分别饮用双蒸水、50、100和200 mg,/L醋酸铅溶液。水迷宫测试20 d龄仔鼠学习能力;Y迷宫测试20、40、60 d龄仔鼠主动学习和记忆能力。结果 仔鼠水迷宫错误次数随母鼠铅暴露剂量增加而增加,100和200 mg/L组明显高于对照组(P<0.05或P<0.01),逃避潜伏期只有高剂量组长于对照组(P<0.05)。各剂量组仔鼠Y迷宫0 min、10 min和24 h逃避达标率20 d龄时最低,停止接触铅以后有所恢复,到60 d龄时达最高;在60 d龄时各剂量组仔鼠的10 min逃避达标率与对照组差异无显著性(P>0.05),而100和200mg,/L组0 min、24 h逃避达标率仍显著低于对照组(P<0.05或P<0.01)。结论 母体铅暴露先损伤仔鼠的学习和记忆能力,其次损伤运动能力。停止铅暴露后短时记忆能力恢复较好,学习、长时记忆能力恢复较差。     

Severe postnatal iron deficiency alters emotional behavior and dopamine levels in the prefrontal cortex of young male rats

Iron deficiency in early human life is associated with abnormal neurological development. The objective of this study was to evaluate the effect of postnatal iron deficiency on emotional behavior and dopaminergic metabolism in the prefrontal cortex in a young male rodent model. Weanling, male, Sprague-Dawley rats were fed standard nonpurified diet (220 mg/kg iron) or an iron-deficient diet (2-6 mg/kg iron). After 1 mo, hematocrits were 0.42 ± 0.0043 and 0.16 ± 0.0068 (mean ± SEM; P < 0.05; n = 8), liver nonheme iron concentrations were 2.3 ± 0.24 and 0.21 ± 0.010 μmol/g liver (P < 0.05; n = 8), and serum iron concentrations were 47 ± 5.4 and 23 ± 7.1 μmol/L (P < 0.05; n = 8), respectively. An elevated plus maze was used to study emotional behavior. Iron-deficient rats displayed anxious behavior with fewer entries and less time spent in open arms compared to control rats (0.25 ± 0.25 vs. 1.8 ± 0.62 entries; 0.88 ± 0.88 vs. 13 ± 4.6 s; P < 0.05; n = 8). Iron-deficient rats also traveled with a lower velocity in the elevated plus maze (1.2 ± 0.15 vs. 1.7 ± 0.12 cm/s; P < 0.05; n = 8), behavior that reflected reduced motor function as measured on a standard accelerating rotarod device. Both the time on the rotarod bar before falling and the peak speed attained on rotarod by iron-deficient rats were lower than control rats (156 ± 12 vs. 194 ± 12 s; 23 ± 1.5 vs. 28 ± 1.6 rpm; P < 0.05; n = 7-8). Microdialysis experiments showed that these behavioral effects were associated with reduced concentrations of extracellular dopamine in the prefrontal cortex of the iron-deficient rats (79 ± 7.0 vs. 110 ± 14 ng/L; P < 0.05; n = 4). Altered dopaminergic signaling in the prefrontal cortex most likely contributes to the anxious behavior observed in young male rats with severe iron deficiency.     

Comparison of alcohol-preferring (P) and nonpreferring (NP) rats on tests of anxiety and for the anxiolytic effects of ethanol

Rats of the selectively bred alcohol-preferring P and alcohol-nonpreferring NP lines were evaluated using three different behavioral measures of anxiety. Compared with NP rats, P rats (1) showed greater footshock-induced suppression of operant responding in an approach-avoidance conflict test; (2) spent less time in the open arms of an elevated plus maze; and (3) took longer in a passive avoidance test to step down from a platform to a grid floor where footshock was received 24 hours earlier. These findings indicate a greater degree of anxiety in the P than in the NP line of rats in these situations. Pretreatment with intraperitoneal (IP) ethanol (0.5–1.0 g/kg) injections produced anticonflict or anxiolytic effects in P but not in NP rats. However, the anticonflict effects of ethanol were small relative to those produced by chlordiazepoxide (CDP, 7.5 mg/kg) in both lines. The results demonstrate that selective breeding for divergent oral ethanol preference has produced associated differences between the P and NP lines of rats in behavioral tests of anxiety and in the anxiolytic effects of ethanol.     

母亲情绪症状与学龄前儿童情绪行为问题的关联

目的 探讨母亲情绪症状与学龄前儿童情绪行为问题的关联,为预防和干预学龄前儿童情绪行为问题提供参考。方法 采用分层整群抽样方法,于2021年6月选择安徽省阜阳市3个区12所幼儿园4 100名3～6岁儿童为研究对象,通过长处和困难问卷(SDQ)、抑郁-焦虑-压力量表(DASS-21)分别调查学龄前儿童情绪行为问题和母亲情绪症状。结果 学龄前儿童情绪症状、品行问题、多动、同伴交往问题、亲社会行为、困难总分异常的检出率分别为15.7%,17.4%,20.0%,32.3%,15.1%和15.8%,母亲抑郁、焦虑、压力症状的检出率分别为7.9%,12.7%,4.8%。多因素Logistic回归分析结果显示,与母亲无抑郁、焦虑、压力症状的儿童相比,母亲有抑郁、焦虑、压力症状的儿童情绪症状、品行问题、多动、同伴交往问题和困难总分异常检出率均增大(OR=1.76～6.35,P值均<0.01),其中母亲情绪症状对儿童情绪症状的影响作用最大,而母亲有压力症状与儿童亲社会行为的关联无统计学意义(OR=1.40,P>0.05)。母亲情绪症状与儿童情绪行为问题关联的性别差异无统计学意义(ROR=0.7...     

孕前慢性应激后仔鼠学习记忆与胰岛素样生长因子Ⅱ表达相关性研究

[目的]观察孕前慢性应激后仔鼠学习记忆能力与海马中胰岛素样生长因子Ⅱ（insulin-like growth factor-Ⅱ,IGF-Ⅱ）的表达变化,探讨仔鼠学习记忆能力变化的机制。[方法]建立慢性应激孕期大鼠模型,通过血浆皮质酮动态测定来检测模型,采用Morris水迷宫和Y迷宫进行学习记忆能力测定、实时荧光定量聚合酶链式反应（real-timepolymerase chain reaction,RT-PCR）检测海马中IGF-Ⅱ表达水平。[结果]模型组母鼠血浆皮质酮水平增高（P〈0.05）;模型组仔鼠只数及母鼠孕天数均少于对照组（P〈0.05）,两组雌雄比例差异无统计学意义（P〉0.05）;模型组仔鼠血浆皮质酮高于对照仔鼠组（P〈0.05）;模型组仔鼠学习、记忆能力低于对照组（P〈0.05）;模型组仔鼠IGF-ⅡmRNA表达量低于对照仔鼠组（P〈0.05）。[结论]孕前慢性应激后仔鼠空间学习记忆能力下降,可能与其脑内IGF-Ⅱ表达的下调及体内皮质酮升高有关系。     

Learning behavior in rat offspring after in utero and lactational exposure to either TCDD or PCB126

Objectives We studied and compared the possible effects of in utero and lactational exposure to 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) or 3, 3′, 4, 4′, 5-pentachlorobiphenyl (PCB126) on learning behavior in offspring. Methods Pregnant Long–Evans Hooded rats were administered either TCDD (50, 200, or 800 ng/kg) or PCB126 (500, 2,000 or 8,000 ng/kg) on gestational day 15. A procedure of schedule-controlled operant behavior was applied to examine learning behavior in the male and female offspring at 11 weeks of age for 30 days. Three indices, namely, response rates in a fixed ratio (FR) and in a differential reinforcement of low rates (DRL), and reward rate in the DRL component in multiple FR 20 DRL 20 s (mult-FR 20 DRL 20-s) test sessions, were used for the evaluation of learning behavior. Results Toxic effects on learning behavior in male and female pups following in utero and lactational exposure to TCDD or PCB126 were observed mainly in the FR learning component. However, no linear dose-dependent effects of either of the two compounds were observed for the above three indices. The response rates of animals in the low-dose TCDD and PCB126 groups decreased and those in medium-dose TCDD and PCB126 groups appeared to induce hyperactive behavior. The high dose of PCB126 appeared to have a distinct toxicity from that of TCDD in terms of the acquisition of learning behavior. Conclusions Toxicities of PCB126 and TCDD in learning behavior might be similar to each other and the current toxic equivalency factor (TEF) of 0.1 for PCB126 can be considered to be appropriate for this endpoint.