大鼠孤束核神经降压素在迷走—加压反应中的作用

采放放射免疫、核团微量注射及组织荧光分光测定等实验方法,研究了大量孤束核神经降压素对迷走－加压反应的影响,结果表明,１．不走神经向中端,孤束核神经降压素免疫活性物的含量明显增高;２．孤束核内注入抗神经降压素血清后,刺激颈迷走神经向中端,迷走－加压反应明显;３．孤束核内注入神经降压素后,刺激颈迷走神经向中端,迷走－加压反应明显减弱,４．孤束核注入神经降压素后,刺激颈迷走神经向中端,孤束核去甲腺素含量     

大鼠蓝斑核对血压和迷走加压反应的影响

我们观察电刺激大鼠蓝斑核对血压和迷走—加压反应的影响,其结果简述如下:一、电刺激大鼠单侧蓝斑(17只)及双侧蓝斑(27只)均引起明显的加压反应,后者更为显著。二、同时电刺激蓝斑核与迷走神经向中端引起极明显的加压反应。三、损毁垂体及切除双侧肾上腺届,蓝斑加压反应明显减弱。四、烧毁双侧蓝斑核,迷走—加压反应消失。据此我们认为迷走一加压反应可能包含蓝斑核所释放的去甲肾上腺素的作用。     

脑室注射纳洛酮对大鼠迷走-加压反应的影响

本文研究了太鼠的迷走-加压反应和脑室注射纳洛酮对大鼠迷走-加压反应的影响。其结果为:1.刺激大鼠迷走神经向中端,可出现迷走-加压反应;2.脑室注射纳洛酮15—20分钟左右,大鼠迷走-加压反应显著抑制;50分钟左右抑制效应解除,迷走-加压反应开始复现。以上事实提示:内源性阿片样物质参与大鼠的迷走-加压反应过程,对迷走-加压反应可能起加强作用。     

猫颈部和腹部迷走神经加压反应的比较研究

刺激麻醉猫颈部和腹部迷走神经中枢端引起的升压反应,不但反应模式有别,其升压机制也不同。颈部迷走加压反应是在出现快速降压之后的一个缓慢持续的血压升高,而腹部迷走加压反应则是一个快而短暂的升压反应。在颈迷走加压反应出现的同时伴有血浆加压素(AVP)的增加,但血浆肾素活性(PRA)及血管紧张素 Ⅱ(ANG Ⅱ)和肾神经放电(RND)都有不同程度的下降。腹部迷走加压反应的出现则伴有 RND,PRA 和血浆 ANG Ⅱ 水平的增加,但 AVP 无明显改变。兴奋同一迷走神经颈腹段传入纤维引起的升压效应之所以不同主要是由于传入纤维的来源和在中枢的投射部位不同,因而升压机制也各异。     

刺激大鼠迷走神经向中端对其不同脑区5-HT含量的影响

采用荧光分光光度法,测定脑内5-HT的含量,观察电刺激两侧颈迷走神经向中端对大鼠海马、下丘脑和中-桥脑内5-HT含量的影响,结果如下:(1)刺激迷走神经向中端后,三脑区的5-HT含量均显著增加(P<0.05-0.005);(2)侧脑室内注射新斯的明(10μg/10μl)或烟碱(10μg/10μl)后,刺激迷走神经向中端使三脑区5-HT含量增多的效应显著提高(p<0.01-0.001);(3)侧脑室内注射六烃季胺(250μg/10μl)后,刺激迷走神经向中端使三脑区5-HT含量增多的效应显著下降(p<0.05-0.005);(4)侧脑室内注射阿托品(10μg/10μl)或纳洛酮(10μg/10μl)后,不影响刺激迷走神经向中端引起的三脑区5-HT含量增多的效应(p>0.05)。由此看来,迷走传入冲动很可能先使脑内Ach释放增多,然后,Ach作用于N-胆碱受体而导致海马、下丘脑和中-桥脑内5-HT含量增加。以上结果表明,在脑内,迷走传入纤维和5-HT能神经元之间可能存在着机能联系。     

迷走传入的投射区在电刺激颈迷走神经中枢端引起的降压反应中的作用

文献报道迷走传入直接或间接投射至多个脑区。本工作分别检验这些脑区在迷走传入引起的降压、降心率反应中的作用。在乌拉坦麻醉、双侧切断颈迷走神经的大鼠,将普鲁卡因微量注入孤束核或β-内啡肽抗血清注入延髓头端腹外侧区(RVL)均可明显减小电刺激预迷走神经中枢端引起的降压(DpV)和降心率反应,但分别将心得安、β-内啡肽抗血清注入室旁核或普鲁卡因注入最后区对DpV和心率减慢反应均无明显影响。保留右侧颈迷走神经的大鼠,在甲基阿托品(i.v.)阻断心迷走神经作用后DpV亦无明显变化,但心率减慢反应被衰减。鉴于我们以往的实验显示孤束核可通过其β-内啡肽能投射纤维作用于RVL而起降压作用,以上结果提示:迷走传入通过孤束核的β-内啡肽能神经元对RVL-交感兴奋神经元起抑制作用是引起降压反应的机制之一。     

纳洛酮对家兔迷走-加压反应的影响

本文观察了刺激家兔颈迷走神经中枢端所引起的加压反应(迷走-加压反应)和侧脑室内注射纳洛酮对家兔迷走-加压反应的影响,结果表明:刺激家兔颈迷走神经中枢端而引起的加压反应可为侧脑室注射纳洛酮后而抑制,这提示内源性阿片样物质参与家兔的迷走-加压反应过程。     

切除肾上腺后的迷走——垂体加压反应

张锡钧等(1937、1938)自发现垂体后叶能因迷走神经的反射刺激而分泌加压素后,复证实催产素亦可因同样机制而分泌。谢维铭(1938)显示刺激迷走神经中枢端所引起的血醣增加,为加压素的另一功能。吕运明等(1965)报道刺激狗、猫、羊、猪的迷走神经向中端均可引起血压升高反应(以下简称:迷走-加压反应)。切除垂体或两侧肾上腺,再刺激迷走神经向中端,血压仍升高。二者完全切除后,加压反应消失,但有时仍出现微弱的加压反应。等(1961,1964,1965,)在急性猫实验中,刺激其迷走神经向中端,血压出现双杷图形,在颈内动脉注射乙酰胆碱(以下简称Ach)可得同样结果,切除     

迷走传入的投射区在电刺激颈走神经中枢端引起的降压反应中的作用

文献报道迷走传入直接或间接投射至多个脑丘。本工作分别检验这些脑区在迷走传入引起的降压,降心率反应中的作用。在乌拉坦麻醉、双侧切断颈迷走神经的大鼠,将普鲁卡因微量注入孤束核β－内啡肽抗血清注入延髓头端腹外测区均可明显减小电刺激颈迷走神经中枢引起的降压和降心率反应,但分别将心得安,β－内啡肽抗血清注入室旁核或普鲁卡因注入最后区对Ｄｐｖ和心率减慢反应均无明显影响,保留右侧颈迷走神经的大鼠,在甲基阿托品（     

刺激家兔腹部迷走神经外周端降压效应中枢机制的研究

应用电解损毁和脑室内注射药物的方法研究了刺激家兔腹部迷走神经外周端所致降压效应的中枢机制。结果表明:1.电刺激延脑闩部尾侧1.5—2mm、中线旁开0.25mm、深1—2mm 处主要引起降压反应。2.电解损毁该部位可以使刺激腹部迷走神经外周端所引起的降压效应显著减弱(n=20,P<0.001),但对刺激减压神经所致降压反应无影响。3.在延脑闩部水平电解损毁减压神经纤维在孤束核的主要投射区可以使刺激减压神经所致降压反应显著减弱,而对刺激腹部迷走神经外周端所致降压反应无影响。4.第四脑室注射5,6-双羟色胺的动物较之注射人工脑脊液的动物颈、胸髓5-羟色胺含量明显降低、动物动脉压增高、心率明显增快、刺激减压神经所致降压反应未见减弱,而刺激腹部迷走神经外周端所致降压反应却明显减小。因此,我们认为家兔腹部迷走神经外周端所致降压效应依赖于延脑闩下部的中缝隐核及连合核等结构,而与减压神经的投射部位无关。延脑中缝核至脊髓的下行性5-HT能神经纤维抑制脊髓交感节前神经元的活动,是这个降压效应的中枢机制之一。     

Locus coeruleus is a central chemoreceptive site in toads

The locus coeruleus (LC) has been suggested as a CO2 chemoreceptor site in mammals. This nucleus is a mesencephalic structure of the amphibian brain and is probably homologous to the LC in mammals. There are no data available for the role of LC in the central chemoreception of amphibians. Thus the present study was designed to investigate whether LC of toads (Bufo schneideri) is a CO2/H+ chemoreceptor site. Fos immunoreactivity was used to verify whether the nucleus is activated by hypercarbia (5% CO2 in air). In addition, we assessed the role of noradrenergic LC neurons on respiratory and cardiovascular responses to hypercarbia by using 6-hydroxydopamine lesion. To further explore the role of LC in central chemosensitivity, we examined the effects of microinjection of solutions with different pH values (7.2, 7.4, 7.6, 7.8, and 8.0) into the nucleus. Our main findings were that 1) a marked increase in c-fos-positive cells in the LC was induced after 3 h of breathing a hypercarbic gas mixture; 2) chemical lesions in the LC attenuated the increase of the ventilatory response to hypercarbia but did not affect ventilation under resting conditions; and 3) microinjection with acid solutions (pH = 7.2, 7.4, and 7.6) into the LC elicited an increased ventilation, indicating that the LC of toads participates in the central chemoreception.     

谷氨酸钠兴奋室旁核引起的升压效应及其与蓝斑-升压反应和A_1-降压反应间的关系

将L-谷氨酸钠(Glu)注入乌拉坦麻醉、箭毒化、人工呼吸大鼠的室旁核(NPV)或蓝斑内引起升压反应。蓝斑升压反应可被双侧室旁核内预先注射酚妥拉明或心得安明显衰减;双侧室旁核内预先注射酚妥拉明或荷包牡丹碱还可使Glu兴奋延髓A_1区引起的降压反应减小,但注射心得安对A_1-降压反应无明显影响。以上结果提示蓝斑-升压反应和A_1-降压反应均部分通过NPV实现,A_1降压过程中可能有NPV内GABA能抑制性中间神经元参与。     

Somatodendritic α2-Adrenoceptors in the Locus Coeruleus Are Involved in the In Vivo Modulation of Cortical Noradrenaline Release by the Antidepressant Desipramine

Abstract: The effect of the antidepressant and selective noradrenaline reuptake blocker desipramine (DMI) on noradrenergic transmission was evaluated in vivo by dual-probe microdialysis. DMI (1, 3, and 10 mg/kg, i.p.) dose-dependently increased extracellular levels of noradrenaline (NA) in the locus coeruleus (LC) area. In the cingulate cortex (Cg), DMI (3 and 10 mg/kg, i.p.) also increased NA dialysate, but at the lowest dose (1 mg/kg, i.p.) it decreased NA levels. When the α₂-adrenoceptor antagonist RX821002 (1 µ M ) was perfused in the LC, DMI (1 mg/kg, i.p.) no longer decreased but rather increased NA dialysate in the Cg. In electrophysiological experiments, DMI (1 mg/kg, i.p.) inhibited the firing activity of LC neurons by a mechanism reversed by RX821002. Local DMI (0.01–100 µ M ) into the LC increased concentration-dependently NA levels in the LC and simultaneously decreased NA levels in the Cg. This decrease was abolished by local RX821002 administration into the LC. The results demonstrate in vivo that DMI inhibits NA reuptake at somatodendritic and nerve terminal levels of noradrenergic cells. The increased NA dialysate in the LC inhibits noradrenergic activity, which in part counteracts the effects of DMI on the Cg. The modulation of cortical NA release by activity of DMI at the somatodendritic level is mediated through α₂-adrenoceptors located in the LC.     

Morphine and beta-endorphin antagonize posture and locomotor disorders induced by the injection of ACTH 1-24 in the rat locus coeruleus

The unilateral microinjection of ACTH 1-24 (20 nmol) into the locus coeruleus (LC) produced a long lasting (2-3 hr) posture asymmetry and movement disorder in all rats tested. This response was readily suppressed by the subsequent local microinjection of an equimolar dose of beta-endorphin or morphine or by the intraperitoneal injection of morphine sulphate (50 mg/kg). Microinjection of naloxone (20 nmol) into the LC produced the above syndrome in a lower percentage of animals. The results support the hypothesis that ACTH peptides and opioids play opposite roles in the control of different brain functions.     

ON THE ORIGIN OF VANILLYLMANDELIC ACID AND 3-METHOXY-4-HYDROXY-PHENYLGLYCOL IN THE RAT BRAIN

Abstract— The effects of electrothermic destruction and electrical stimulation of the locus coeruleus on the brain levels of vanillylmandelic acid (VMA), 3-methoxy-4-hydroxyphenylglycol (MOPEG) and noradrenaline (NA) were studied in the rat. Fourteen days after destruction of the locus coeruleus, the content of NA in the hippocampus and that of MOPEG in the rest of the brain were decreased by more than 70% and 50% respectively.
Stimulation of the locus coeruleus induced a decrease in hippocampal levels of NA of 38%, while MOPEG levels were found to be increased more than 3-fold After intraventricular injection of 1 μg of adrenaline (A), the levels of MOPEG were Substantially increased In none of these experiments was any variation in VMA levels found, These results suggest that in the rat brain endogenous VMA is not a metabolite of either NA or A The formation of MOPEG from A as well as from NA appears to be possible.     

蓝斑核对上呼吸道阻力肌—颏舌肌功能的影响

本实验在３８只经氨基甲酸乙酯麻醉的健康家兔上进行,观察了电、化学刺激蓝斑核（ＬＣ）对颏舌肌功能的影响。结果如下：（１）长串电脉冲刺激蓝斑核使颏舌肌肌电活动明显增强,表现为长吸性肌电积分幅度升高,膈肌亦出现与颏舌肌同步的肌电活动增强。（２）ＬＣ内微量注射胞体兴奋剂谷氨酸钠,也引起明显的颏舌肌和膈肌肌电活动增强。（３）上述电、化学刺激的区域对照和盐水对照实验,均未出现有意义的肌电改变。提示：电、化学刺激ＬＣ可特异性增强上呼吸道阻力肌──颏舌肌的紧张性活动,具有减小上呼吸道阻力的作用,这对于某些上呼吸道阻塞性疾病发病机制的研究可能具有重要的意义。     

Aδ afferent fiber stimulation activates descending noradrenergic system from the locus coeruleus

We compared the noradrenaline (NA) level in the dorsal horn following electrical stimulation of Aδ afferent nerve fibers in the peripheral nervous system between rats with bilateral lesions of the locus coeruleus (LC) and non-operated control rats by using a microdialysis technique combined with high performance liquid chromatography. Prior to Aδ afferent fiber stimulation, the NA content in the dialysate did not differ between the LC-lesioned and the control rats. During Aδ afferent fiber stimulation, in the LC-lesioned rats, the NA level did not change significantly compared to that before Aδ afferent fiber stimulation, whereas the NA level increased significantly in the control rats. There was a significant difference in the NA levels during Aδ afferent fiber stimulation between the two groups of rats. The result suggests that descending noradrenergic neurons from the LC is involved in the increase of the NA level in the spinal cord dorsal horn produced by Aδ afferent fiber stimulation.     

慢性应激性高压大鼠中刺激弓状核引起的压作用

Hypertension was induced by chronic foot-shock and noise stress in adult male Sprague-Dawley rats. Microinjection of 0.3 microliters (150 mmol) sodium glutamate (Glu) into the nucleus arcuatus (ARC) elicited a significant depressor effect in rats with chronic stress-induced hypertension. The depressor effect induced by excitation of ARC neurons was attenuated significantly by microinjection of 0.3 microliters beta-endorphin antiserum (beta-EPAS) into the dorso-medial periaqueductal gray (PAG) or 0.1 microliters into the area of locus coeruleus (LC) due to blockage of beta-endorphinergic fibres from ARC to PAG or LC.     

蓝斑在刺激视上核镇痛中的作用

应用核团微量注射、放射免疫测定（ＲＩＡ）和高压液相（ＨＰＬＣ）观察了刺激视上核（ＳＯＮ）对蓝斑（ＬＣ）灌流液中催产素（ＯＴ）、精氨酸加压素（ＡＶＰ）、去甲明上素（ＮＥ）和５－羟色胺（５－ＨＴ）的含量的变化以及斑注射Ｏ笔ＡＶＰ的拮抗剂对痛阈（ＰＴ）的影响。结果表明;刺激ＳＯＮ后３０到９０ｍｉｎ,ＬＣ灌流液中ＯＴ的含量,３０ｍｉｎＡＶＰ的含量,６０ｍｉｎ５－ＨＴ的含量明显增加,而ＮＥ的含量在３０和６０