本文分析了大鼠延髓头端腹外侧区(RVLM) 神经元单位电活动与心血管活动的相干性, 观察了RVLM区神经元电活动对电刺激中脑防御反应区的诱发反应, 以及对压力感受性反射的反应。并用FFT对RVLM区神经元自发单位放电和血压波进行频域的相干性分析, 以判断是否具有心节律。还分析了RVLM区单位放电变异性与心率变异性的相干性。结果显示: RVLM区大多数神经元对电刺激中脑防御反应区呈兴奋反应(67%), 70%神经元放电活动被注射苯肾上腺素而升高的动脉血压强烈抑制, 具有心节律的神经元占64%, 50%神经元放电变异性与心率变异性的高频呈良好的相关。神经元电活动的频谱分析为深入研究心血管自主神经系统功能提供了一种新方法。

目的　研究嘌呤能受体(purinergic receptors,P2) 家族中P2X 不同亚型在新生和成年SD大鼠延髓的表达。方法　成年SD大鼠(6-8w) 和新生SD大鼠(1-5d)，各6只,雌雄不计，取延髓。应用免疫组织化学的方法和图像分析技术，比较P2X2和P2X4受体在新生和成年SD大鼠延髓的表达。结果　P2X2和P2X4嘌呤受体的阳性神经元和阳性纤维在新生鼠和成年鼠的延髓都有广泛表达，主要分布在孤束核、Ⅻ颅神经核和延髓腹外侧区，延髓其他区域为散在的分布。成年鼠和新生鼠的P2X2受体均比P2X4受体表达水平高。在新生鼠髓,P2X2 和P2X4的表达水平均比成年鼠低。结论　P2X2 和P2X4阳性神经元和阳性纤维广泛分布在大鼠延髓,为ATP对心血管活动、呼吸活动和痛觉等的调节作用提供了结合位点,也有利于实验中P2X受体亚型阻断剂的选择。随着动物发育成熟,P2X2和P2X4表达水平均增加。

采用微量注射、微透析、高效液相色谱-荧光测定等技术和方法，观察和分析了血管紧张素-(1-7)[Ang-(1-7)]在延髓头端腹外侧（RVLM）与氨基酸类递质释放之间的关系。在麻醉大鼠RVLM注射Ang-(1-7)可引起血压升高，同时伴RVLM兴奋性氨基酸（EAA）释放增多：在RVLM注射Ang-(1-7)选择性受体拮抗剂Ang779可引起血压降低，同时伴RVLM EAA释放减少和抑制性氨基酸（IAA）释放增多。Ang-(1-7)的升压作用和Ang779的降压作用均可被相应的氨基酸受体拮抗剂部分阻断。结果提示，Ang-(1-7)在RVIM的升压效应可能部分是通过EAA释放增多而致；而Ang779在RVLM的降压效应可能部分是通过EAA释放减少，IAA释放增多所致。

The goal of this study was to determine the origin and transmission pathway of respiratory drive to hypoglossal motoneurons. First we recorded intracellularly from 28 antidromically activated inspiratory hypoglossal motoneurons (resting membrane potential, -50

采用逆转录-聚合酶链式反应检测了慢性足底电击结合噪声应激致高血压大鼠下丘脑、延髓、中脑、垂体和肾上腺等组织中编码肾上腺髓质素的肾上腺髓质素前肽原(preproadrenomedullin, ppADM) 基因以及ADM 的特异性受体组件降钙素受体样受体(calcitonin-receptor-like receptor，CRLR)和受体活性调节蛋白2和3(receptor-activity- modifying proteins, RAMP2 和RAMP3) 表达的变化。我们观察到：与对照组相比，以3- 磷酸甘油醛脱氢酶作为内参照，15d足底电击结合噪声应激引起下丘脑、垂体和肾上腺中ppADM mRNA表达上调，而在延髓和中脑表达明显下调(P<0.01 或 P<0.05); CRLR 基因表达量正常时在下丘脑相对较高，应激15 d 后CRLR 表达在延髓、中脑和下丘脑下调(P<0.01 或 P<0.05), 而在垂体和肾上腺的表达无明显变化；应激后RAMP2 基因在延髓和下丘脑表达上调，而在肾上腺表达显著下调(P ＜ 0.01), 其他部位无明显变化；RAMP3 基因在对照组大鼠的中脑和下丘脑表达较高，在应激性高血压大鼠的下丘脑和垂体表达上调(P<0.01 或P<0.05), 而在中脑和肾上腺表达下调(P<0.05), 在延髓中的表达变化无统计学差异。上述结果提示：慢性足底电击结合噪声应激引起明显的中枢和下丘脑- 垂体- 肾上腺轴ADM 及其受体组件CRLR/RAMP2 或CRLR/RAMP3 基因的表达变化。但慢性应激后中枢源性ADM 及其受体的表达变化对应激和血压的调节以及在应激致高血压中的确切作用及机制尚待进一步研究。

采用多管微电泳结合细胞外记录的方法研究了肾上腺髓质素(adrenomedullin, ADM)对大鼠延髓头端腹外侧区(rostral ventrolateral medulla, rVLM)压力反射敏感性神经元电活动的作用及其可能机制。结果显示：在29 个rVLM压力反射敏感神经元中，20个神经元在30、60 和90 nA 的电流微电泳大鼠ADM (rADM)过程中，放电频率由(10.8±2.7) spikes/s分别增加到(14.6±3.6)、(19.8±4.7)和(31.9±6.4) spikes/s(P<0.05，n=20)。微电泳rADM特异性受体阻断剂人ADM (human ADM, hADM) (22-52)可明显减小神经元放电频率的增加幅度，比正常放电频率仅增15.4％ [(11.4±2.5) sipkes/s, P<0.05, n=10]，而降钙素基因相关肽1 (CGRP1)受体阻断剂hCGRP (8-37)对rADM兴奋性神经元电活动影响较小。在另外23个神经元中，10个神经元的放电频率在10、20 和40 nA 电流微电泳神经型NOS(nNOS)抑制剂7-NiNa 过程中放电减少，由正常的(10.1±3.5)spikes/s分别减少为 (7.5±2.5)、(5.3±2.1)和(3.1±1.4) spikes/s (P<0.05, n=10)。在微电泳7-NiNa 过程中同时微电泳rADM，则rADM增加神经元放电频率的效应减弱，增加幅度为基础水平的17％ [(6.2±1.9) spikes/s]。8个神经元在10、20 和40 nA电流微电泳诱导型NOS 抑制剂(iNOS) aminoguanidine (AG)过程中放电频率由(11.5±5.1) spikes/s 增加到(17.8±5.6)、(22.5±6.3)和(29.1±6.4) spikes/s (P<0.05, n=8)，rADM 与AG 同时微电泳时，AG对rADM本身增加神经元放电的效应无明显影响。上述结果提示，rADM在rVLM可通过其特异性受体或来源于nNOS 的NO作用于压力反射敏感神经元，使其活动增强而发挥调节心血管活动的作用。

The main source of expiratory drive to respiratory muscles in the rat is thought to be the caudal expiratory neurones. However, their projections to the spinal cord and the coordination of the population activity with the respiratory cycle are largely unknown. We examined their bulbospinal projections using antidromic activation, and the coordination of their activity using crosscorrelation. Of 76 expiratory neurones examined, 40% projected to the C2 segment of the spinal cord, all unilaterally and all but 4 to the contralateral side. Thirteen contralateral axons were located in the ventromedial funiculus, when activation thresholds were less than 25 μA. For 29 neurones, the mean (±SEM) conduction velocity, calculated from the single-point activation and a measure of the direct distance between recording and stimulating electrodes, was 7.4±0.4 m/s. We calculated 88 crosscorrelograms from ipsilateral pairs of expiratory neurones recorded on the same side of the medulla, and 176 contralateral pairs recorded from opposite sides of the medulla. All of the latter were featureless, but 23% of cross-correlograms for ipsilateral pairs displayed broad peaks at time zero, which we interpreted as due to activation of both neurones from a common source. We conclude that in the adult rat, approximately half of the caudal expiratory neurones project unilaterally and contralaterally to the spinal cord and, although common activation serves to coordinate some of the ipsilateral population, we suggest that neither common activation nor excitatory cross-connections exist as sufficient means for coordinating left and right populations to the same respiratory rhythm.

Expiratory neurones, with a decrementing firing pattern during the first phase of expiration (EDEC) and located in the rostral ventrolateral medulla, are thought to be involved in the network generating respiratory rhythm, which also includes expiratory neurones with augmenting firing patterns (E-AUG). We used crosscorrelation to detect their synaptic interconnections and connections to phrenic motoneurones in 32 vagotomised, decerebrate, paralysed and ventilated male rats. Pairs of neurones were recorded extracellularly with glass-insulated tungsten microelectrodes and the whole phrenic nerve with bipolar silver wire electrodes. Of the 79 crosscorrelograms computed between pairs of E-DEC neurones, 8 (-10%) showed evidence for inhibitory connections. Of the 67 cross-correlograms computed between EDEC and E-AUG neurones, 5 (7.5%) showed evidence for a monosynaptic inhibition of the E-AUG neurone by the E-DEC neurone, while 3 (4.5%) showed evidence for a monosynaptic inhibition of the E-DEC neurone by the EAUG neurone. An inhibitory connection from E-DEC neurones to phrenic motoneurones was detected in 5 (-2%) of the cross-correlograms, and from E-AUG neurones to phrenic motoneurones in 4 (-3.7%). These results are the first demonstration that network models of rhythm generation in the rat involving reciprocal inhibition between E-DEC and E-AUG neurones could have a neurophysiological basis, and the first to demonstrate that phrenic motoneurones are inhibited during the early phase of expiration by E-DEC neurones.

在α2氯醛糖麻醉的猫上, 结扎左心室冠状动脉前降支(LAD)一小分支, 对动物胆囊浆膜面予以缓激肽(BK), 可反射性地诱发血压、左心室内压升高、±dP/dtmax增大、心率加快,同时用超声单晶片声纳测微系统记录局部心壁运动, 发现BK可以反射性地引起LAD小分支远端所支配的心肌运动功能减弱。电针内关穴对BK诱发的升压反应有抑制作用, 并可改善局部心肌运动功能。静脉注射纳洛酮(014mg/kg) 能翻转电针效应。结果表明, 电针能够抑制BK诱发的升压反应和改善局部心肌运动功能, 该效应与内源性阿片肽有关。