不同生殖状态雌性大鼠下丘脑视上核和室旁核内一氧化氮合酶神经元的变化

为了探讨下丘脑视上核 (SON)和室旁核 (PVN)内的一氧化氮 (NO)水平与生殖活动的关系 ,本实验应用 NADPH-黄递酶组织化学和 NOS免疫组织化学 ,研究了妊娠期、哺乳期和正常雌性大鼠 SON和 PVN内 NO合酶 (NOS)神经元的变化规律。结果发现 ,妊娠期大鼠的 NOS神经元数目、胞体截面积和免疫反应产物的灰度值在 PVN分别为 49.8± 3.9、15 2 .4± 14.1μm2 和 15 3.4± 8.9;在 SON分别为 2 9.2± 3.7、 16 3.5± 13.8μm2 和 140 .5± 7.2。 SON和 PVN的前两项指标均显著高于正常大鼠 (P<0 .0 1) ,而灰度值显著低于正常大鼠 (P<0 .0 1)。哺乳期大鼠 PVN的 NOS神经元数目和胞体截面积分别高于正常大鼠 2 8%和 9% ,而灰度值低于正常大鼠 7% ;在 SON,则分别高 75 %、 11%和低 9% ,以上三项指标均有显著性差异 (P<0 .0 1)。哺乳期大鼠 SON的 NOS神经元数目亦显著高于妊娠期大鼠 (P<0 .0 1)。这些结果提示 ,雌性大鼠在妊娠期和哺乳期 ,其 SON和 PVN内的 NOS活性上调     

CHRONIC LYSERGIC ACID DIETHYLAMIDE ADMINISTRATION AND SEROTONIN TURNOVER IN VARIOUS REGIONS OF RAT BRAIN

—Acute injections of LSD (2 × 500 μg/kg) to rats resulted in evidence of a reduced 5-hydroxytryptamine (5-HT) turnover in all brain areas studied. In contrast, a much smaller dose of LSD (20 μg/kg) repeated daily for 1 month produced a significantly reduced turnover only in the midbrain area. The pons/medulla and forebrain areas showed small and not statistically significant increases in 5-HT turnover.     

长时程冷暴露后大鼠下丘脑脑片视前区温敏神经元的适应性变化

本文比较了生活在冷室（５±１℃，２０只）和暖室（２０±３℃，３５只）达三周的雄性Ｗｉｓｔａｒ大鼠下丘脑脑片视前区神经元电活动和温度敏感性，共记录到１２７个来自暖室组及８６个来自冷室组自发放电神经元。结果表明：（１）冷适应后冷敏神经元的比例明显提高，温度敏感性不变而放电活动的临界温度和下限温度明显下移；（２）热敏神经元的温度敏感性和临界温度降低，但在３７℃时的自发放电活动频率显著增加；（３）非温敏神经元的电活动也增加，其下限温度下移极显著，显示了大鼠视前区神经元在冷适应中的可塑性及其与冷适应中体温调节的机制相关。     

BRAIN SEROTONIN CHANGES IN PHENYLALANINE-FED RATS: SYNTHESIS STORAGE AND DEGRADATION1

The brain serotonin levels of rats maintained on a 5 % phenylalanine diet rose more slowly (0.18 μ g/g brain/hr) after administration of a monoamine oxidase inhibitor than did serotonin levels of controls (0.41 μ g/g brain/hr). The rate of brain serotonin decline following reserpine or dimethylaminobenzoyl methyl reserpate was the same for both groups as was basal monoamine oxidase activity. Brain uptake of monoamine oxidase inhibitor was also the same for both groups. It was concluded that the decrease in brain serotonin levels in phenylalanine-fed animals was due to decreased serotonin formation rather than enhanced degradation. On the basis of available data it was concluded that both hydroxylase inhibition and inhibited precursor transport were involved.     

DNA TURNOVER IN ADRENAL MEDULLARY CELLS OF DIFFERENT STRAINS OF RATS AND ITS ENHANCEMENT AFTER INTERMITTENT EXPOSURE TO COLD

In Italico and Wistar rats maintained at room temperature 1% of nuclei of cells in the adrenal medulla incorporate ³H-thymidine. Following intermittent exposure to cold, the numbers incorporating increase to 10% and 7% in Italico and Wistar strains respectively. Only in the Wistar strain does the increase occur during actual exposure.
Assuming S to be 6–8 hr the labelling indices actually determined indicate a turnover time of DNA of 21–29 days. Since mitotic indices in experimental and control animals were found to be 0.004% without colchicine treatment and 0.009% after 3 hr of colchicine treatment, the turnover times of cells were calculated to be 1388–3125 days. To correlate mitotic indices and labelling indices, an S period of 400 hr would have to be assumed. It is concluded therefore that: (i) most of the observed labelling of DNA is due to metabolic turnover of DNA and only a small proportion represents pre-mitotic synthesis, (ii) differences in the rates of DNA synthesis found during exposure to cold in Italico and Wistar rats respectively are sufficient to account for the differences in reduction of DNA previously found between the two strains under these experimental conditions.     

CHANGES IN THE DNA CONTENT OF ADRENAL MEDULLA NUCLEI OF RATS INTERMITTENTLY EXPOSED TO COLD

In the adrenal medulla of rats exposed intermittently to cold (+4°C) for 100 and 300 hours, a considerable decrease (24 to 40 per cent) of the DNA content per nucleus was observed, followed by restoration to normal or above normal values within 10 days after the withdrawal of the stimulus. The findings were obtained with a scanning integrating histophotometer, and confirmed by microinterferometric investigations (on the basis of the measurement of total dry mass of nuclei isolated in aqueous medium before and after treatment with DNase) and by microchemical determinations, combined with the count of the nuclei in the homogenates. The observed decrease of DNA content cannot be attributed to errors of the methods used, nor to consequences of cellular degeneration. The available evidence seems to indicate a real decrease rather than a change in the state of a part of DNA in the nucleus in vivo whereby it becomes extractable by aqueous solutions. The restoration cannot be due to mitotic processes, which were actually never detected even with the use of colchicine, since the adrenal medulla cells in the adult rat are known to be irreversible, postmitotic cells. A correlation between the functional activity of the adrenal medulla cells and the content or state of DNA in their nuclei is demonstrated.     

性腺甾体激素对雌,雄大鼠下丘脑血管升压素mRNA水平的影响

实验用１０－１１周龄经阉割的雌、雄Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠进行。以３末端异羟基洋地黄毒甙标记的２６个碱基长的寡核苷酸作为检测探针,用核酸斑点杂交技术检测大鼠下丘脑血管升压素ｍＲＮＡ水平。在假手术对照组,雄性大鼠下丘脑ＡＶＰｍＲＮＡ水平经雌性大鼠高４５％（Ｐ〈０．０５）,血浆渗透压高于雌性大鼠（Ｐ〈０．０５）。摘除卵巢的大鼠下丘脑ＡＶＰｍＲＮＡ深恶痛绝经假手术组雌性大鼠高３０％（Ｐ〈０．０５     

慢性缺氧对大鼠肺组织中G_(α0)的分布及基因表达的影响

为研究Ｇ蛋白变化与慢性缺氧性肺动脉高压发生的关系,本文应用核酸分子杂交方法及免疫组织化学法,测定了慢性缺氧性肺动脉高压大鼠肺组织Ｇ蛋白（Ｇα０）ｍＲＮＡ水平及其在肺组织中的分布。结果发现：Ｇα０分布于肺动脉壁肌层的神经纤维中,慢性缺氧可使Ｇα０阳性神经纤维数目明显增多,而且肺组织中Ｇα０ｍＲＮＡ水平为对照组的１．６８倍。结果提示：慢性缺氧性肺动脉高压发病过程可能有通过Ｇα０起作用的神经机制参与     

磁场对丘脑下部一氧化氮含量的影响及与丘脑下部神经内分泌核团的关系

应用硝酸还原酶反应—分光光度法测定和NADPH-d组织化学技术,对磁场处理后丘脑下部一氧化氮量的变化及其可能的原因进行了研究,发现磁场可促使丘脑下部一氧化氮量(OD值)显著升高,并具有显著滞后效应。NADPH-d阳性神经细胞及NADPH-d和血管加压素(AVP)双染阳性神经细胞集中分布在丘脑下部室旁核、室周核和视上核,但不存在 于视交叉上核,提示室旁核、室周核和视上核一氧化氮能神经细胞是丘脑下部的一氧化氮的主要来源。磁场处理后大鼠丘脑下部一氧化氮含量(OD值)较正常对照组显著升高应归因于这些神经细胞受磁场作用表达增强。一氧化氮和血管加压素的共存可能对磁场调节内分泌具有一定意义。     

大鼠侧脑室慢性注射CRF致抑郁样变化研究

为了探讨CRF在抑郁症发生发展过程中的作用．对正常大鼠侧脑室慢性注射CRF21天并与慢性非预见性应激刺激21天建立的抑郁症模型大鼠进行比较。运用旷场行为实验（open-field）观察大鼠主动性活动能力．用Morris water Maze法．以训练期的逃避潜伏期为指标检测大鼠空间学习记忆能力。采用HPLC—UV法测定血清皮质醇含量,RT—PCR法检测CRF及其受体mRNA的表达。结果显示：慢性应激21天建立的模型大鼠主动性活动和学习记忆能力均明显下降．血清皮质醇含量显著升高,CRF及其受体R1 mRNA的表达增加。大鼠侧脑室慢性注射CRF21天后．其体重增量、主动性活动和学习记忆能力与慢性应激模型大鼠一样均明显降低。这些工作证明了CRF在抑郁症的发生发展过程中发挥了至关重要的作用．慢性应激导致机体CRF分泌持续增加可能是抑郁症发病的主要原因。     

CHANGES IN CENTRAL NORADRENALINE NEURONSADMINISTRATION AFTER SYSTEMIC 6-HYDROXYDOPAMINE ADMINISTRATION

—Intravenous injection of a large dose of 6-hydroxydopamine (100 mg/kg) to adult rats caused a significant and long-lasting reduction (about 30 per cent) of the in oirro uptake of [³H]NA in the cerebral cortex and spinal cord, while no changes were seen in the hypothalamus. The endogenous NA in whole brain was similarly reduced (about 20 per cent). Fluorescence histochemistry revealed catecholamine accumulations which are degenerative signs, induced by 6-hydroxydopamine, in axons of the dorsal NA bundle innervating the cerebral cortex. It is concluded that the blood–brain barrier in adult rats is not completely protective with respect to the neurotoxic action of systemically injected 6-hydroxydopamine, which can produce degeneration of a significant number of NA nerve terminals in the cerebral cortex and spinal cord. Previous studies have shown that 6-hydroxydopamine caused a permanent and selective degeneration of a large number of central NA nerve terminals when injected systemically up to 1 week after birth, due to an incompletely developed blood-brain barrier. This barrier for 6-hydroxydopamine develops between the 7th and 9th day after birth (Sachs , 1973). In the present study 6-hydroxydopamine was found to cause a small transient reduction in [³H]NA uptake in cerebral cortex of rats between 9 and 28 days of age, while in older rats the damage produced by 6-hydroxydopamine was long-lasting. Thus, the NA nerves ascending to the cerebral cortex seem to possess a regenerative capacity to a 6-hydroxydopamine-induced degeneration up to about 28 days postnatally, but which later disappears or is markedly retarded.     

电磁脉冲辐照大鼠海马区细胞凋亡与形态学变化

以体外原代培养的大鼠海马神经元和Wistar大鼠为研究对象,探讨电磁脉冲(场强为6× 104 V/m)辐照后早期海马区细胞凋亡和病理形态学的变化.在照射后1h、6h、12h、24h和48h分别采用MTT法和流式细胞仪测定死亡细胞和凋亡细胞的比例,用光镜和电镜分别进行形态学观察.结果显示在电磁脉冲辐照后,海马神经细胞不仅发生快速的坏死,而且还发生凋亡,同时在早期即可见到血管、胶质细胞和神经元等组织的形态学异常.表明大鼠大脑受电磁脉冲辐照后早期海马区可发生神经细胞坏死和凋亡,以及各组织成分的病理形态学改变,上述变化可能与电磁脉冲致细胞DNA损伤有关.     

兴奋下丘脑弓状核神经元降低大鼠血浆唾液酸水平的作用

实验采用下丘脑弓状核（ＡＲＣ）区微量注射和紫外分光光度测定法,研究ＡＲＣ区注射不同浓度谷氨酸钠（Ｇｌｕ）对大鼠血浆唾液酸（ＳＡ）水平的影响。结果表明：（１）ＡＲＣ区注射Ｇｌｕ后,血浆ＳＡ水平较对照组明显降低（Ｐ〈０．０１）,而且随Ｇｌｕ浓度的增加,血浆ＳＡ水平降低所需的时间逐渐缩短;（２）侧脑室注射阿朴吗啡后,ＡＲＣ区注射Ｇｌｕ,血浆ＳＡ水平明显降低（Ｐ〈０．０１）,而且降低发生时间较对照组提前：     

ESR研究急性运动及恢复期大鼠RBCM脂流动性的改变

本文以大鼠递增负荷力竭性运动为模型,利用电子自旋共振（ＥＳＲ）技术测定急性运动中及不同时程恢复期红细胞膜（ＲＢＣＭ）脂流动性的改变。ＲＢＣＭ脂尾部流动性在短时间中等强度运动（三级负荷末）即有明显下降（Ｐ＜０．０５）,在运动后恢复期进行性加重,并于运动后１２ｈ达极显著改变（Ｐ＜０．０１）：此时膜脂头部流动性也明显下降（Ｐ＜０．０５）。之后二者均有恢复趋势,提示递增负荷力竭性运动对ＲＢＣＭ脂流动性有重要影响,并且ＲＢＣＭ脂流动性与膜功能相互作用,互相影响     

大鼠下丘脑室旁核-下丘脑前区(PVH-AHA)神经元对电刺激丘脑束旁核(PF)的逆行反应和顺行反应

本工作以逆行鉴定的方法研究了丘脑束旁核(PF)和下丘脑室旁核-下丘脑前区(PVH-AHA)之间的神经连接。在 PVH-AHA 观察了150个神经元对 PF 刺激的反应。其中,7个单位发生逆行反应,42个单位发生顺行反应,101个单位没有反应。逆行反应的潜伏期为10—12ms,传导速度约0.4m/s.顺行刺激和逆行刺激的结果表明 PF 与 PVH-AHA 之间存在着交互连接。     

褪黑素对谷氨酸钠致痫大鼠脑内一氧化氮含量的影响

目的观察褪黑素(Melatonin,MT)对谷氨酸钠致痫大鼠脑内一氧化氮(nitric oxide,NO)含量的影响,研究其抑制癫痫的作用机制。方法40只健康雄性SD大鼠随机分为4组(每组10只):生理盐水对照组(NS组);谷氨酸钠致痫组(Glu组);褪黑素+谷氨酸钠组(MT+Glu组);Luzidole+褪黑素+谷氨酸组(Luz+MT+Glu组)。观察大鼠行为变化,记录脑电图,用NADPH组织化学反应检测大鼠海马内NO含量变化。结果行为学观察和EEG显示,NS组无痫样发作和痫样放电,Glu组和Luz+MT+Glu组痫样发作重(Ⅲ-Ⅴ级),脑电图显示频发高幅的痫样波,MT+Glu组有轻微发作(0-Ⅱ级),脑电图上偶见散在单个微小痫样波;NADPH组织化学反应结果显示,Glu组和Luz+MT+Glu组大鼠大脑皮质及海马内NOS阳性细胞与对照组比较增多,差异性明显(P<0.05),MT+Glu组较Glu组和Luz+MT+Glu组内NOS阳性细胞减少,差异性明显(P<0.05)。结论MT对谷氨酸钠致痫大鼠痫样发作程度、痫样放电有抑制作用,其机制之一是经其特异性受体,减弱NO作用,进而发挥抑痫效应。     

急性给锂小鼠大脑皮层NOS活性与蛋白表达的时程变化

目的探讨急性给锂小鼠大脑皮层一氧化氮合酶(NOS)活性与蛋白表达的时程变化及其意义.方法选用昆明小鼠40只,分为对照组和腹腔注射1.5mmol/Kg氯化锂(LiCl)即刻、0.5h、1h、3h、6h、12h、24h组,每组5只.采用NADPH-d黄递酶组织化学和ABC免疫组化法,观察急性给锂后不同时程小鼠大脑皮层NOS和nNOS阳性神经元数目的变化.结果急性给锂即刻小鼠大脑皮层NOS和nNOS阳性神经元数目明显增加(P＜0.01),1h后达到高峰(P＜0.01),6h和12h恢复到正常水平(P＞0.05),24hNOS阳性神经元又明显增高(P＜0.01),nNOS阳性神经元处于正常水平(P＞0.05).结论本实验提示急性给锂对小鼠大脑皮层NOS和nNOS阳性神经元数目有一定影响,这种变化可能是锂影响脑发育及锂的神经毒性的机理之一.     

口服醋酸棉酚前后人精子体外受精能力及精核转变的细胞学观察

本文报道口服醋酸棉酚对人精子体外受精能力、原核及染色体形成的影响。结果表明,在口服醋酸棉酚前的9名男性精子对金黄地鼠卵的穿透率平均为62%。每日口服20mg醋酸棉酚15天后,精子对卵的穿透率下降至47%,30天后下降至24%,50天后下降至8%。即口服醋酸棉酚50天后达到了不再具有生殖能力的精子穿透率阈值(10%)以下。原核及染色体形成的观察表明,即使口服醋酸棉酚50天后,仍可见有完整原核的形成,并未见有明显的染色体畸变。综述上列结果,似乎表明口服醋酸棉酚虽可影响人精子对去除透明带金黄地鼠卵的穿透率,而进入卵内的精子仍可形成原核及染色体。因此,仅从成熟精子的生理功能而论,口服醋酸棉酚期间它似乎并不产生可察觉的致畸效应,这与醋酸棉酚对体细胞并无致畸作用的报道相一致。     

早期干预改善缺氧缺血性脑损伤大鼠认知能力及其机制分析

目的研究早期干预对缺氧缺血性脑损伤(HIBD)大鼠学习记忆功能的影响及其作用机制。方法选用SD大鼠建立宫内HIBD动物模型,随机分为非干预组和干预组,非干预组与正常对照组常规饲养,对干预组采取早期触摸和丰富环境刺激。干预28d后,通过三等臂Y型迷宫试验检测各组大鼠的学习记忆功能,而后取大鼠额皮质和海马组织进行病理观察,并采用DNA缺口原位末端标记法(TUNEL反应法)检测凋亡细胞,观察脑组织神经元凋亡情况。结果单纯HIBD组大鼠学习获得与记忆保持能力明显低于正常对照组(P<0·01),但HIBD干预组Y迷宫测试成绩则优于HIBD非干预组(P<0·01)。同时,HIBD非干预组脑额皮质和海马CA1区神经元缺失远较正常组多(P<0·01),而HIBD干预组与HIBD非干预组之间神经元数量的差异则不那么显著。但HIBD干预组脑额皮质和海马神经元凋亡百分率明显低于HIBD非干预组(P<0·01)。结论早期干预可减轻缺氧缺血性损伤脑组织神经细胞凋亡,该作用可能是早期干预促进HIBD大鼠脑功能修复的机制之一。