中枢5—HT1A受体在大鼠脑中的不同亲和力状态

用特异性配体［＾３Ｈ］８－ＯＨ－ＤＰＡＴ与大鼠脑中不同部位脑组织膜制剂的５－ＨＴ１Ａ受体结合，显示出在海马、延髓、下丘脑的最大结合容量和亲和力有明显不同。各种孵育缓冲液使鼠脑海马、延髓膜制剂与［＾３Ｈ］８－ＯＨ－ＤＰＡＴ的结合呈现乐同的亲和力状态。孵育缓冲液中加入Ｍｎ＾２＋和Ｇｐｐ（ＮＨ）ｐ或均不加时，结合呈高、低两种亲和力状态；而仅加入Ｍｎ＾２＋或同时加入ＥＤＴＡ和Ｇｐｐ（ＮＨ）ｐ时，结合分别呈     

自发性高血压大鼠不同脑区5－HT_（1A）受体的结合特征

用放射性配基［~３Ｈ］８－ＯＨ－ＤＰＡＴ结合实验显示，自发性高血压大鼠（ＳＨＲ）脑区的海马、延髓、下丘脑５－ＨＴ_（１Ａ）受体的结合位点明显高于正常ＷｉｓｔａｒＫｙｏｔｏ（ＷＫＹ）大鼠，其中海马增加最多。在此基础上用抗高血压药普萘洛尔给ＳＨＲ灌胃，结果其脑区不同部位受体结合参数、血压及心率都有不同程度的变化，更接近于ＷＫＹ大鼠。这说明ＳＨＲ与ＷＫＹ大鼠之间不同脑区５－ＨＴ_（１Ａ）受体特异性差别可能与高血压的发病有关。     

大鼠中枢5-HT1A受体的结合容量与高血压

目的:探讨5-HT1A受体结合容量改变对高血压发病的影响.方法:通过放射性配体与受体结合实验,探讨不同周龄自发性高血压大鼠(SHR)和对照组Wistar-Kyoto (WKY)大鼠在脑区不同部位5-HT1A受体的结合特征.结果:SHR不同脑区脑组织膜的Bmax随着大鼠周龄的增加而增大,且有显著差异;WKY鼠差异不明显.相同脑区不同周龄SHR的Bmax均大于WKY大鼠,且随着周龄的增加血压呈上升趋势,其5-HT1A受体的Bmax与血压成正比,WKY无此现象.4～5周龄的SHR为高血压未形成期,10～12及以上周龄的SHR处于高血压的形成期.结论:当血压发生变化时,中枢5-HT1A受体结合容量发生继发性改变.不同脑区中枢5-HT1A受体结合容量可能与高血压疾病的发生相关.     

大鼠中枢内源性镇痛系统内GABAB受体与5-HT共存神经元的观察

目的：观察GABAB受体（GABABR）与5－HT在大鼠中脑导水管周围灰质（PAG）,中缝核簇和巨细胞网状核a（部（GiA)神经元内的共存,方法：GABABR和5－HTGABABR5－HT和GABA特异性抗体的免疫荧光组织化学双重及三重染色技术,结果：GABABR／5－HT双标神经元胞体较密集地见于中缝背核,中缝正中核,中缝桥核,中缝大核,中缝苍白核,中缝隐核,此外,PAG和GiA内也可见双标神经元,GABA样阳性终末与GABABR／5－HT双标神经元的胞体和树突形成密切接触,结论：PAG,K中缝核簇和GiA内的5－HT能神经元几乎均呈GABABR样阳性,GABA能终末与GABAB受体／5－HT双标神经元形成密切接触,GABA可能通过GABAB受体调节5－HT能神经元的活动,参与对伤害性信息传递的的调控。     

内皮素A受体拮抗剂BQ_（123）预防内皮素－1的致心律失常作用

探明内皮素－１（ＥＴ－１）致心律失常作用的受体机制。方法：雄性ＳＤ大鼠３５只经冠状动脉口注射内皮素Ａ受体拮抗剂ＢＱ１２３，观察其对ＥＴ－１致心律失常作用的影响。结果：ＢＱ１２３０．１１～７μｇ／ｋｇ预处理后再注射ＥＴ－１引起的心律失常严重程度、发生率、死亡率呈剂量依赖性降低。ＢＱ１２３为７μｇ／ｋｇ时心律失常记分（ＡＳ）降为０，与ＥＴ－１对照组比较有非常显著差异（Ｐ＜０．０１）。结论：ＥＴ－１的致心律失常作用很可能是通过ＥＴＡ受体而介导的。     

大鼠脑加压素受体测定方法的建立

采用~(125)碘标记精氨酸加压素(~(125)I-AVP),建立了大鼠脑粗制膜上AVP受体的测定方法。结果表明,第一次冻融可使~(125)I-AVP与脑粗制膜上受体的结合率降低约35％,第二次冻融则降低约70％。用此方法测得大鼠脑粗制膜上AVP受体的最大结合容量Bmax为157.1±16.3fmol/mg蛋白,平衡解离常数Kd为0.25±0.04nmol/L。     

5羟色胺1A(5-HT_(1A))受体参与调制大鼠丘脑中央下核5-HT诱发的抗伤害感受效应

目的:研究5-HT1A受体是否参与调节中虫下核(Sm)内由5-HT引起的抗伤害效应。方法:以辐射热诱发浅麻大鼠甩尾(TF)反射潜伏期为痛反应指标,在Sm内单独微量注射5-HT1A受体拮抗剂。结果:5-HT1A受体拮抗剂p-MPPI(0.87nmol)可易化TF反射,小剂量的p-MPPI(0.43nmol)可明显减弱Sm内注射5-HT后引起的甩尾(TF)反射抑制效应。结论:5-HT1A受体参与调制大鼠丘脑中央下核5-HT诱发的抗伤害感受效应。     

NMDA受体NR2B亚基在脑微血管内皮细胞模型中作用机制研究

神经精神性狼疮(neuropsychiatric lupus erythe-matosus,NPSLE)发病机制尚不完全清楚,目前认为,NPLE与多种自身抗体及细胞因子异常有关,NMDA受体是中枢神经系统兴奋性氨基酸(EAA)离子型受体,它过度兴奋或抑制都会导致细胞凋亡,狼疮病人血清中抗NR2a和NR2b抗体水平与特定的脑功能损伤有关,本研究旨在比较抗NR2抗体与NMDA受体拮抗剂、激动剂对脑微血管内     

Effect of cyproheptadine on changes of 5-HT and 5-HIAA levels in brain cortex and serum following rat brain injury

Changes of 5-hydroxytryptamine(5-HT)and 5-hydroxyindoleacetic acid(5-HIAA)levels in brain cortex and serum were studied using spectrofluorometer follow-ing brain injury in rats.Cyproheptadine,a receptor antagonist of 5-HT,was employedand its effect on alterations of 5-HT and 5-HIAA contents in brain cortex and serum af-ter brain injury was investigated.The results showed that after brain injury levels of5-HT and 5-HIAA in the brain cortex increased markedly,The increase of 5-HT in thebrain cortex reached its peak at 48h after brain injury,and its value was 4.29±0.44μg/g,which was 4.8 times of control value.The increase of 5-HIAA in the brain cortexreached its peak at 24h after brain injury,and its value was 5.48±0.41μg/g,which was5.8times of control value.The change of 5-HT in the serum was not significant,but thelevel of 5-HIAA in the serum was increased significantly.Cyproheptadine could reducelevels of 5-HT and 5-HIAA in this experiment.The value of 5-HT in the brain cortexdecreased to 1.32±0.09μg/g,and the value of 5-HIAA decreased to 1.36±0.10μg/g.Thelevel of 5-HIAA in the serum was also reduced significantly.It was 0.27±0.03μg/ml.     

氰化物对大鼠脑单胺类递质的影响

大鼠腹腔注射NaCN中毒后3,5、10、30、45和60min用荧光法分别测定脑内多巴胺(DA)、去甲肾上腺素(NE)、5-羟色胺(5-HT)和5-羟吲哚乙酸(5-IHAA)含量。结果表明,中毒后脑内以上4种单胺含量呈剂量依赖性下降,45min时,低剂量NaCN(2.36mg/kg)中毒动物脑内DA和NE含量显著升高。氰化物中毒惊厥时伴有脑内单胺类递质含量的显著降低。提示脑内单胺类递质的变化在氰化物中枢毒理作用中可能具有重要意义。     

Study on glucocorticoid receptor of brain cytosol in rats with traumatic brain edema

The high-affinity glucocorticoid binding sites(HAGS)and the low-affinity glucocor-ticoid binding sites(LAGS)with steroid specificity were demonstrated in cerebral cytosol ofrats by using the radioligand binding assay.The equilibrium dissocation constant(Kd)of HAGSand LAGS were(2.78+0.71)×10~(-8)mol/L and(2.12±1.06)×10~(-6)mol/L respectively as esti-mated by Scatchard and Pseudoseatchard analysis.Glucocorticoid receptors(GR)in the trau-matized(left)hemisphere cytosol were decreased more significantly than those in both the con-trol(right)hemisphere cytosol at 6 h postinjury and normal brain tissue(P<0.05),but Kd ofGR showed no significant changes.GR of liver cytosol at 6h postinjury were more markedly de-creased than normal hepatic cytosol,but Kd of GR underwent no significant changes.These da-ta demonstrate that high-dose glucocorticoid(GC)used in the treatment of traumatic brain ede-ma might maintain target-cell reactions by increasing the production of GC receptor complexesand is most likely to be mediated by LAGS.     

应激对大鼠胃窦及十二指肠5-HT细胞内5-HT含量的影响

本实验采用免疫组化及显微分光扫描测定法,观察了浸水拘束性应激刺激对大鼠胃窦及十二指肠5-羟色胺(5-HT)细胞内5—HT含量的影响.实验结果表明,浸水拘束性刺激8 h后,实验组5只大鼠的瘤胃全部发生溃疡,但十二指肠未见溃疡发生,正常对照5只大鼠均无溃疡发生.对应激组大鼠的胃窦切片进行5-HT细胞扫描,发现5只大鼠的胃窦5—HT细胞内5—HT明显增加.应激组n=100(细胞数)为0.506±0.058 AU(为随意单位值),明显高于正常对照组0.460±O.070 AU P<0.01.相反,应激组大鼠十二指肠内5-HT细胞的5-HT含量明显降低.对照组为0.380±0.007 AU,应激组为0.350±0.040 AU,P<0.01.此结果提示胃窦内源性5—HT可能与应激性溃疡的形成有关.     

强啡肽A_（1－13）与大鼠急性脑创伤后脑水肿的关系

观察强啡肽Ａ１－１３（ＤｙｎＡ１－１３）与脑创伤后脑水肿的关系。方法：采用放免方法与密度梯度脑水肿测定方法。结果：ＤｙｎＡ１－１３含量，伤侧皮质除伤后４ｈ显著高于对照组外，伤后２，１０与２４ｈ都显著低于对照组，伤侧海马伤后４个时间点均显著低于对照组，下丘脑伤后１０，２４ｈ明显低于对照组；组织密度伤后４ｈ伤侧海马与皮质明显低于对照组，伤后２４ｈ降低最为明显；海马的ＤｙｎＡ１－１３含量与组织密度呈正相关；侧脑室注射ＤｙｎＡ１－１３可减轻脑水肿，而注射ｋ受体拮抗剂ｎｏｒ－ＢＮＩ则可加重脑水肿。结论：强啡肽Ａ１－１３的减损可能是脑创伤后脑水肿形成的显著因素，它对脑创伤后脑水肿具有潜在的治疗价值。     

Experimental study on alteration of adrenergic receptors activity in neuronal membranes protein of cerebral cortex following brain trauma in rats

Objective: To define the course of changes taken by α1 and β adrenergic receptors (AR) activity after traumatic brain injury (TBI) and explore the approach for secondary brain injury (SBI) management. Methods: The neuronal membrane protein of cortex were extracted from the rats subject to traumatic brain injury, and the changes of α1- and β-AR activities in the neuronal membranes were examined by radio ligand binding assay (RLBA). Results: α1- and β-AR activities underwent obvious changes, reaching their peak values at 24 h after TBI. α1-AR binding density (Bmax) reduced by 22.6%while the ligand affinity increased by 66.7%, and for β-AR, however, Bmax increased by 116.9% and the ligand affinity reduced by 50.7%. Their antagonists could counteract the changes ofα1- and β-AR activity. Conclusion: The patterns of changes varies between α1- and β-AR activity after TBI, suggesting their different roles in the neuronal membranes after brain trauma, and timely administration of AR antagonists is potentially beneficial in TBI management.