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1.
精氨酸加压素对大鼠抗体产生和淋巴细胞增殖的上调作用   总被引:5,自引:0,他引:5  
Bai HB  Du JZ  Zheng XX 《生理学报》1999,51(4):435-438
大鼠侧脑室注射100ng精氨酸加压素(AVP),用ELISA法检测血中对鸡卵白 白抗原产生的IgG抗体水平。结果显示,IgG水平高于对照,而AVP的V1受体阻断剂DPAVP则可阻断此作用;icv800ngAVP,大鼠的SRBC溶血素 水平高于对照;icv100ng、800ngAVP2h后,脾淋巴细胞对MTT产生的颜色反应均比对照增加,而DPAVP可阻断之;icv800AVP2h后,脾淋巴细胞对MT  相似文献   

2.
隔区不仅分布大量的精氨酸加压素 (AVP)神经元 ,而且也分布温敏神经元 ,参与生理性与行为性体温调节。本文观察了侧脑室注射AVP和微电泳AVP对隔区温敏神经元放电活动的影响 ,以证明隔区注射AVP的抗热作用是否与AVP直接影响 ,隔区温度敏感神经元的活动有关。1 材料与方法选用体重 1 8~ 2 6kg家兔 36只 ,用 2 5 %乌拉坦溶液静脉麻醉 (1 g/kg) ,完成有关手术。用直流恒温电热毯裹住家兔躯体 ,使肛温维持在 38 5℃。隔区温敏神经元放电活动的记录定位按Sawyer兔脑图谱取A3~ 5,L1~ 2 5,H5~ 9(脑表面下 …  相似文献   

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杏仁内侧核注射AVP和AVPMcAb对家兔ET性发热效应的影响   总被引:2,自引:0,他引:2  
目的和方法:在大脑杏仁内侧核微量注射精氨酸加压素(AVP)和精氨酸加压素单克隆抗体(AVPMcAb),观察其对家兔内毒素(ET)性发热效应以及视前区一下丘脑前部(POAH)温敏神经元放电活动的影响。结果:①杏仁内侧核微量注射AVP能明显抑制家兔ET性发热效应,注射AVPMcAb能明显易化家兔ET性发热效应;②杏仁外侧核分别注射AVP和AVPMcAb则对家兔ET性发热效应无明显影响;③杏仁内侧核分别注射AVP和AVPMcAb后POAH热敏神经元和冷敏神经元放电活动均无明显变化。结论:家兔杏仁内侧核也是AVP抗热效应的一个重要的作用部位,杏仁内侧核注射AVP的抗热作用途径与隔区注射AVP的抗热途径可能不同  相似文献   

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家兔脑内P物质介导侧脑室注射乙酰胆碱的心血管效应   总被引:1,自引:0,他引:1  
大量工作表明 ,乙酰胆碱 (acetylcholine ,ACh)广泛分布于中枢心血管控制核团 ,参与正常血压的调节 ,且与原发性高血压的发生、发展有关。但是 ,关于脑内ACh在整体水平对心脏收缩功能的直接影响 ,国内外尚未见报道。P物质 (substanceP ,SP)是一种神经肽 ,广泛存在于中枢神经系统 ,作为一种神经递质或调质参与心血管活动的调节 ,中枢应用SP可产生与ACh相一致的升压效应。有资料表明 ,ACh与SP在大鼠桥脑共存于同一个神经元。那么 ,ACh和SP在中枢心血管活动调节中的相互关系如何呢 ?目前。国内…  相似文献   

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精氨酸加压素(AVP)的C端内片段,AVP(4-8),具有增强记忆的功能,它在大鼠脑内引发一系列的生理和生化变化。GTP-结合调节蛋白(G蛋白)介导多数神经肽和神经调质的细胞内生理生化反应,放射性受体结合实验显示,在海马突触膜上存在AVP(4-8)的特异性结合位点。AVP(4-8)在海马突触膜上的结合能够进一步刺激GTPγS结合并可被AVP(4-8)的受体拮抗剂ZDC(C)PR所逆转。从以上实验结  相似文献   

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本研究旨在了解弓状核内的阿片受体在体温调节中的作用。研究使用细胞介素IL1β做致热源。以自动推进器向SD雄性大鼠弓状核微量注射1μ1IL1β。在给药前30min分别向弓状核微量注射通常阿片受体拮抗剂纳洛酮(Nal)、阿片受体μ、δ和κ各自特异性拮抗剂CTAP、NTI和norBNI做预处理,用生理盐水(Sal)做对照。结果表明:IL1β所致的升体温效应能被Nal和CTAP阻断,提示弓状核中的阿片受体(主要是μ受体)参与或介导了IL1β的致热效应;δ和κ受体特异性拮抗剂阻断IL1β所致的体温升高效应不明显。提示δ和κ阿片受体参与体温调节的可能性较小。对照ARH和POAH中阿片受体在IL1β所致发热中的作用可发现:二者作用极为相似,这一结果有力地支持了弓状核是体温调节中枢重要组成部分的观点。  相似文献   

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目的:观察5-羟色胺1A (5-HT1A)受体阻断剂p-MPPI对乙醇引起大鼠低体温和行为性体温调节反应的影响。方法:用无线遥控测温技术记录成年雄性SD大鼠体核温度和活动的变化。用无线遥测温度梯度仪监测大鼠体核温度和行为性体温调节活动,将大鼠置于15℃~40℃的温度梯度箱内,并允许动物自由选择箱内温度,观察乙醇(3 g/kg)引起低体温和行为性体温调节的反应以及5-HT1A受体阻断剂p-MPPI (1 mg/kg)对其效应的影响。结果:①乙醇能引起大鼠快速的体温降低反应,同时动物选择较低的环境温度。②5-HT1A受体阻断剂p-MPPI能明显阻断乙醇引起的低体温和行为性体温调节变化。结论:①乙醇能使体温调定点降低,因为乙醇引起低体温时,大鼠选择较冷环境温度区;②5-HT可能参与乙醇引起低体温与行为性体温调节活动。  相似文献   

8.
AVP(4 ̄8)是精氨酸加压素(AVP)在脑内的天然酶解产物,具有增强学习记忆的功能。为了进一步阐明其作用的分子机制,以SK-N-SH成神经瘤细胞(SK细胞)为模型进行研究。放射性配基结合实验表明,在SK细胞上存在AVP(4 ̄8)的特异性结合位点。AVP(4 ̄8)可以刺激SK细胞中蛋白激酶C(PKC)和促细胞分裂原活化的蛋白激酶(MAPK)尖性的升高,并可以被AVP(4 ̄8)的受体拮抗剂ZDC(C  相似文献   

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促黄体激素/人绒毛膜促性腺激素受体(LH/hCF receptor)是一种与蛋白偶联的糖蛋白。本文报道了从大鼠卵巢cDNA库中筛选LH/hCG受体cDNA及其在昆虫细胞中的高效表达。LH/hCG受体cDNA全长2403bp,编码受体信号肽和成熟受体674个氨基酸。用多角体病毒表达载体pVL1393,LH/hCG受体cDNA在昆虫细胞中得到高效表达。在非还原和还原条件下的SDS-PAGE分析显示,用  相似文献   

10.
电刺激兔肾脏传入神经对血压,心率及加压素释放的影响   总被引:1,自引:0,他引:1  
吕敏  魏顺光 《生理学报》1995,47(5):471-477
本工作以兔为实验对象,观察电刺激肾脏传入神经(ARN)对血压、心率、颈交感神经放电、以及加压素(AVP)合成和释放的影响,并对ARN进入中枢的通路作了观察。结果显示,电刺激ARN可以引起血压下降、心率减慢、颈交感神经放电抑制等反应,ARN的兴奋还可使下丘脑的视上核、室旁核中的AVP含量增加,垂体中AVP含量下降,血浆AVP水平升高。硝普钠的降压实验和静脉注射AVP受体阻断剂AVPa的实验均证实了A  相似文献   

11.
Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.  相似文献   

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In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.  相似文献   

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The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.  相似文献   

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Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.  相似文献   

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