阿片μ受体与SP,CGRP和SOM在大鼠三叉神经节和背根神经节内 …

本研究应用免疫荧光及免疫荧光双重染色技术，观察了大鼠三叉神经节和背根神经节内阿片μ受体免疫反应阳性神经抑的分布及其与ＳＰ，ＣＧＲＰ和ＳＯＭ阳性神经元是是否存在共存关系，结果显示：（１）三叉神经节和背极神经节内的阿片μ受体免疫反应阳性神经元多为中心小型细胞，其免疫反应阳性产物不仅于胞膜表面也出现于胞浆内，ＳＰ和ＳＯＭ免疫反应阳性反应神经亦为中小型细胞，但以小细胞为主，而ＣＧＲＰ免疫反应阳性神经元有一     

大鼠腰骶髓后连合核内5—HT样阳性纤维和终末的来源

采用荧光金（ＦＧ）逆行追踪与免疫荧光组织化学染色相结合技术，对大鼠腰骶髓后连合核（ＤＣＮ）内５－羟色胺（５－ＨＴ）能纤维和终末的分布及其来源进行了观察。结果显示ＤＣＮ内分布有大量５－ＨＴ阳性纤维和终末。将ＦＧ注入到ＤＣＮ后，ＦＧ／５－ＨＴ双标细胞出现于延髓中缝核群中的中缝大核、中缝隐核和中缝苍白核以及外侧旁巨细胞核的腹侧部。结果提示５－ＨＴ对ＤＣＮ内盆内脏感觉信息的传递可能具有调控作用。     

炎性痛大鼠脊髓背角内神经激肽B受体的动态变化

目的：观察神经激肽B受体（NK3）与大鼠髓内伤害性信息和调控的可能关系。方法：用免疫组织化学技术观察完全弗氏佐剂（CFA）诱发慢性性大鼠脊髓背角神经激肽B受体的运动变化。结果：炎症侧腰髓氏脊髓背角NKB受体样免疫反应结构的染色强度有明显升高,背角浅层尤为显著。经进观察与图像分析有明,注射CFA2d后脊髓背角内免疫染色强度即开始升高21d左右抵达高峰,28d后渐恢复至正常水平。结论NKB受体可能参与炎性慢性痛状态下伤害性信息在脊髓水平的传递与整合过程.     

Hijacking Dorsal Raphe to Improve Moods and Metabolism via BDNF Gene Transfer in Mice

Background: Mood disorders such as depression and metabolic diseases like obesity and diabetes have significant comorbidities; furthermore, each disease increases the risk of the other one. Continuing use of antidepressant medication is associated with an elevated risk of type 2 diabetes and weight gain. On the other hand, antiobesity drugs are found to have varying neuropsychiatric adverse event profiles. Therefore, there is an urgent need to develop more effective and safer therapies for mood disorders and metabolic diseases with minimal side effects. Both brain derived neurotrophic factor (BDNF) and serotonin (5-HT) can regulate moods in the limbic system and metabolism in the hypothalamus, respectively. The dorsal raphe nucleus (DR) in the midbrain contains the largest number of serotonin-expressing neurons as well as other neurons expressing various neurotransmitters. Both serotonergic and nonserotonergic DR neurons send projections widely to the forebrain including the limbic system and the hypothalamus. This study aimed to investigate whether BDNF gene transfer in DR neurons can improve moods and metabolism. Methods: Recombinant adeno-associated virus (AAV) was microinjected into DR to achieve BDNF gene transfer. Chronic unpredictable mild stress (CUMS) model of depression in C57BL/6 mice was established to investigate the role of DR BDNF gene transfer in depression. Forced swimming test (FST) and sucrose consumption test (SCT) were used to examine the depressive-like behaviors. Open field test (OPT) and elevated zero maze (EZM) were used to examine the anxiety-like behaviors. Diet-induced obesity (DIO) and leptin receptor mutant db/db mice were employed to investigate the role of DR BDNF gene transfer in regulating metabolism. Metabolic profiling included body weight, food intake, fat mass, serum factors, energy expenditure, glucose tolerance and insulin sensitivity. Quantitative RT-PCR was performed to determine expression changes of several key genes in DR, hypothalamus, liver and fat tissues. Tph2 conditional knockout mice were used to examine whether 5-HT is essential for BDNF in improving metabolism. In addition, chemogenetic activation of DR neurons via AAV-mediated hM3Dq expression was also performed to examine whether there is a similar effect as BDNF. Results: FST and SCT showed significant anti-depressant effects of DR BDNF gene transfer in the CUMS model, meanwhile, OPT and EZM showed significant anxiolytic effects. BDNF gene transfer in DR also markedly ameliorated obesity and hyperglycemia in DIO and db/db mice, which was revealed by lightened body weight, decreased food intake, increased energy expenditure, improved glucose tolerance and insulin sensitivity, reduced levels of serum factors like insulin and leptin. The mRNA expression of genes related to 5-HT signaling such as tph2 and vmat2 was significantly increased in DR after BDNF gene transfer. Expression levels of multiple genes regulating energy balance in the hypothalamus, liver, and fat tissues also changed. Conditional knockout of tph2, encoding the rate-limiting enzyme of 5-HT synthesis, did not block the effects of DR BDNF gene transfer in improving metabolism. Chemogenetic activation of DR neurons also had the effects of improving metabolism in DIO mice. Conclusions: BDNF gene transfer in DR of mice improves moods and metabolism. This study surmounts the “hypothalamocentric” paradigm dominating in metabolism research by connecting metabolism and moods via dorsal raphe.     

猫阴部神经传入传出成分在脊髓内的定位分布—HRP逆行及跨越神经节追踪研究

向猫阴部神经及其分支注入HRP溶液,观察并分析了逆行和跨节追踪的结果。 1.证实阴部神经为含躯体传出、传入,内脏传出、传入纤维的混合神经,其内脏性传出、传入成分仅存在于阴茎背神经中。 2.逆行标记细胞出现于L_7—S_3前角Onuf核和S_(1-3)的中间带外侧核。本文结果表明,Onuf核是支配盆底横纹肌的运动核,但它和其它前角运动核在细胞形态和活性物质的分布上都明显不同。特别是它的一部分神经元的树突形成树突束到达中间带外侧核。本文结合排尿、排便功能从形态学上较详细地讨论了Onuf核和中间带外侧核的关系。 3.本文证明阴部神经领域的内脏初级传入(来自阴茎背神经)和躯体初级传入纤维都向骶髓后连合核区有浓密的投射。结合以往的工作讨论了盆腔脏器、外生殖器的内脏传入和坐骨神经、阴部神经的躯体传入在骶髓后连合核区汇聚的现象及机能意义,推测这种汇聚可能是产生牵涉痛和针刺镇痛机制的形态学基础。     

大鼠脊髓内接受盆腔脏器伤害性刺激神经元的定位分布

本文用Ｆｏｓ蛋白免疫组织化学方法研究了大鼠脊髓内接受盆腔脏器伤害性刺激神经元的分布状况。在对照组，仅偶见Ｆｏｓ阳性细胞出现于Ｌ６、Ｓ１节段脊髓后角（＜２个／片），且染色浅淡。将３％福尔马林经插管分别注入膀胱、阴道和直肠造成伤害性刺激时，Ｆｏｓ阳性细胞数明显增多（１００～２６０个／片，Ｓ１），主要出现于Ｌ６、Ｓ１节段后角Ⅰ层内侧部、后角内侧缘、后连合核和中间带外侧核。少量散在于后角Ⅰ层外侧部、后角外侧缘、外侧脊核和前角背内侧部。为了确定脊髓内Ｆｏｓ阳性神经元是否向上位脑结构投射，将荧光金（ＦＧ）注入一侧臂旁外侧核后，给予膀胱伤害性刺激，结合Ｆｏｓ蛋白免疫组化技术，在后连合核和中间带外侧核发现有ＦＧ／Ｆｏｓ双标细胞。在中间带外侧核，ＦＧ标记细胞与Ｆｏｓ阳性细胞均主要位于核的背侧部，且ＦＧ标记细胞多数同时为Ｆｏｓ阳性，ＦＧ／Ｆｏｓ双标细胞占ＦＧ标记细胞总数的７１．２％（３７／５２），占Ｆｏｓ阳性细胞总数的１４．８％（３７／２５０），提示脊髓内接受盆腔脏器伤害性神经元部分投射至臂旁外侧核。为进一步确定Ｆｏｓ阳性细胞在中间带外侧核定位分布特征，采用ＮＡＤＰＨ脱氢酶反应（显示副交感节前神经元）与Ｆｏｓ蛋白免疫组化相结合?     

影响巴金森氏病神经元死亡的几种因子

<正> 巴金森氏病(PD)主要的神经化学特征是中枢缺失多巴胺(DA)能神经元(Agid etal:Movement Disord 2:166,1987)。但是,DA细胞群并不呈现相同的变性,神经黑色素神经元则易先受累(Hirsh et al,Nature,334,345,1988),提示PD患者的DA能神经元并非均等地受损。事实证明神经元的死亡与内源性和外源性毒性作用有关,并可能伴随超氧化(hyperoxidation)现象。     

—氧化氮合成酶在大鼠腰能髓副交感核、主盆神经节及阴茎勃起组织的分布

本研究用NADPH脱氢酶法观察了大鼠腰骶髓中间带外侧核(IML)、主盆神经节(MPG)及阴茎勃起组织内一氧化氮合成酶(NOS)阳性成分的分布。在L_6、S_1节段的lML内发现有中等大小的阳性神经元,每张切片2～10个。MPG内有大量NOS阳性神经元,染色极深,分布不均匀。以盆神经进入端阳性细胞最密集。占节细胞总数的41.7%。以中小型为主(直径10～30μm,79.1%),阳性纤维分布于节细胞之间。其中既有阳性细胞自身的突起(节后纤     

非创伤性超声波血压测定装置

心脏疾病、糖尿病及脑血管性痴呆等都是由于微循环障碍引起的。因此,了解这些患者的微循环是非常重要的。但现今对直径1mm 以下的微小血管的血压测量,由于插管困难而难以进行,尤其是直径100μm以下的细动静脉及毛细血管。作者应用超声波及电子计算机即时信息处理,非创伤性地测定了从心脏、大血管至微循环等任意部位的血管内压力。本研究主要依据是液体中微小气泡的共振频率依压力变化而改变,压力升高则向高频转变。将比红细胞还小的可通过微循环的弹性胶囊导入目的部位,则胶囊反射从体表进入的超声波,即时接收处理从该部位后方来的散射波而测定血管内压力。在理论上是依据Minnaert 的波动理论即用液体内气泡共振式计算。例如,可忽略不计的直径3μm 的微小气泡)大气压下)及膜压的柔软微胶囊的共振频率为2185.78KMz,该部位如增加1mmHg 的压力,在气体无进出的状态下、胶囊的半径与压力的1/3成反比缩小,共振频率偏移为2188.18KHz。这祥,仅1mmHg 的压力改变,共振频率偏移达2.4KHz,是完全可以检出