Effects of ginkgolide B on neuronal discharges in paraventricular nucleus of rat hypothalamic slices

Objective To study the central role of ginkgolide B （BN52021） in regulating cardiovascular function of nerve center by examining the effects of ginkgolide B on the electrical activity of rat paraventricular nucleus （PVN） neurons in hypothalamic slice preparation and to elucidate the mechanism involved. Methods Extracellular single-unit discharge recording technique. Results （1） In response to the application of ginkgolide t3 （0.1, 1, 10 μmol/L; n = 27） into the perfusate for 2 rain, the spontaneous discharge rates （SDR） of 26 （26/27, 96.30%） neurons were significantly decreased in a dose-dependent manner. （2） Pretreatment with L-glutamate （L-Glu, 0.2 mmol/L） led to a marked increase in the SDR of all 8 （100%） neurons in an epileptiform pattern. The increased discharges were suppressed significantly after ginkgolide B （1 μmol/L） was applied into the perfusate for 2 min. （3） In 8 neurons, perfusion of the selective L-type calcium channel agonist, Bay K 8644 （0.1 μmol/L）, induced a significant increase in the discharge rates of 8 （8/8, 100%） neurons, while ginkgolide B （1μmol/L） applied into the perfusate, could inhibit the discharges of 8 （100%） neurons. （4） In 8 neurons, the broad potassium channels blocker, tetraethylammonium （TEA, 1 mmol/L） completely blocked the inhibitory effect of ginkgolide B （1 μmol/L）. Conclusion These results suggest that ginkgolide B can inhibit the electrical activity of paraventricular neurons. The inhibitory effect may be related to the blockade of L-type voltage-activated calcium channel and potentially concerned with delayed rectifier potassium channel （KDR）.

Hypothalamic paraventricular nucleus stimulation reduces intestinal injury in rats with ulcerative colitis

AIM: To investigate the effect and mechanism of stimulation of the hypothalamic paraventricular nucleus with glutamate acid in rats with ulcerative colitis(UC).METHODS: The rats were anesthetized with 10% chloral hydrate via abdominal injection and treated with an equal volume of TNBS + 50% ethanol enema, injected into the upper section of the anus with the tail facing up. Colonic damage scores were calculated after injecting a certain dose of glutamic acid into the paraventricular nucleus(p VN), and the effect of the nucleus tractus solitarius(NTS) and vagus nerve in alleviating UC injury through chemical stimulation of the p VN was observed in rats. Expression changes of C-myc, Apaf-1, caspase-3, interleukin(IL)-6, and IL-17 during the protection against UC injury through chemical stimulation of the p VN in rats were detected by Western blot. Malondialdehyde(MDA) content and superoxide dismutase(SOD) activity in colon tissues of rats were measured by colorimetric methods. RESULTS: Chemical stimulation of the PVN significantly reduced UC in rats in a dose-dependent manner. The protective effects of the chemical stimulationof the p VN on rats with UC were eliminated after chemical damage to the p VN. After glutamate receptor antagonist kynurenic acid was injected into the p VN, the protective effects of the chemical stimulation of the p VN were eliminated in rats with UC. After AVpVl receptor antagonist([Deamino-penl, val4, D-Arg8]-vasopressin) was injected into NTS or bilateral chemical damage to NTS, the protective effect of the chemical stimulation of p VN on UC was also eliminated. After chemical stimulation of the p VN, SOD activity increased, MDA content decreased, C-myc protein expression significantly increased, caspase-3 and Apaf-1 protein expression significantly decreased, and IL-6 and IL-17 expression decreased in colon tissues in rats with UC. CONCLUSION: Chemical stimulation of the hypothalamic p VN provides a protective effect against UC injury in rats. Hypothalamic p VN, NTS and vagus nerve play key roles in this process.

Mechanism of hypothalamic paraventricular nucleus in regulating asthmatic attack

BACKGROUND:It has been confirmed that c-fos expression increased markedly in hypothalamic paraventricular nucleus(PVN)during asthmatic attack in rats,and PVN has extensive physiological functions,involving in the regulation of respiratory system,etc.OBJECTIVE:To observe the alteration of electroencephalogram(EEG)and power spectra in PVN during the asthmatic attack,and the alteration of lung function and diaphragmatic muscle discharge after bilateral PVN lesion in asthmatic rats.DESIGN:A randomized control study.SETTING:Laboratory of Physiology and Pharmacology,School of Basic Medical Sciences,Southeast University.MATERIALS:Forty-eight male adult SD rats of 260-300 g were used.The rats were randomly divided into 6 groups(n=8):control group,asthma group,electrolytic lesion of PVN group,KA-induced lesion of PVN group,sham electrolytic lesion of PVN group and sham kainic acid(KA)-induced lesion of PVN group.KA,chicken ovalbumin and aluminum hydroxide were purchased from American Sigma Company.Bordetella pertussis vaccine(Institute of Biological Products of Shanghai);stereotaxic apparatus(JiangwanⅡ,China);lesion-producing device(YC-2 programmable stimulato,Chengdu Instrument Company);MD2000 signal processing system(Nanjing Medical School);data acquisition system(RM6240B,Chengdu Instrument Company).METHODs:The experiments were carried out in the Laboratory of Physiology and Pharmacology,School of Basic Medical Sciences,Southeast University from January to August in 2006.①Rats except for control group were sensitized with an intraperitoneal injection of 100 mg chicken ovalbumin and 100 mg aluminum hydroxide and Bordetella pertussis vaccine containing 5×10^(9) heat-killed in 1 mL of sterile saline.From the fifteenth to seventeenth days rats received three times aerosolized ovalbumin challenge.In rats of the control group and asthma group three steel electrodes were placed into the left PVN(AP-1.8 mm,LR 0.4 mm,OH-7.9 mm),parietal cortex and subcutaneous tissue in lower limb.Lung function tests were carried out simultaneously.Small holes were drilled in the skull to introduce a concentric bipolar electrode in the direction of the PVN in order to perform electrolytic lesion.The electrodes were connected to a lesion-producing device and a current of 1.0-1.5 mA was passed over a period of 10-15 s on each side of the PVN.The rats received 0.5μg/0.5μL of KA in phosphate buffer(0.1 mol/L,pH 7.4),and the speed of infusion was 0.1μL per minute in order to perform KA-induced lesion of PVN.②Three days after operation of lesion,lung function tests were carried out.All the electrode and transducer were connected with data acquisition system.This technique yielded airway resistance(Raw),dynamic compliance(Cdyn),the expiratory time(Te)/the inspiratory time(Ti),minute ventilation volume(MVV),EMGdi frequency and EMGdi integral.③The differences of the measurement data were compared using the t test.MAIN OUTCOME MEASURES:①The alteration of EEG and power spectrum of PVN during asthmatic attack in sensitized rats;②The effects of electrolytic lesion or KA-induced lesion of PVN on lung function in asthmatic rats.RESULTS:All the 48 rats were involved in the analysis of results.①Alteration of EEG and power spectrum:Five minutes after injection of ovalbumin into caudal vena,the breathing rate of the rat was obviously speeded up and the total power spectrum was increased[(18476.71±2140.94),(13838.75±2983.26)mV^(2),P<0.01],the percentage of theδpower andθpower decreased significantly(P<0.01),while the percentage ofαpower andβ1 power were enhanced(P<0.05,0.01).Ten minutes after injection,the EEG power spectrum of PVN further shifted rightward,the total power gradually increased(P<0.01)which suggesting that the intensive hypersynchrony activities of PVN neurons.The percentage ofδpower was decreased significantly(P<0.01),but theα,β1 andβ2 were increased(P<0.01).Twenty-five minutes later,the breathing movements became steady,and the EEG power spectrum of PVN returned to the control level step by step.②The alteration of lung function was detected during asthmatic attack after electrolytic lesion or KA-induced lesions of PVN respectively.It was found that EMGdi frequency,Te/Ti and RL were all decreased(P<0.01),EMGdi integral,MVV and Cdyn were all enhanced(P<0.01),while there were no significant changes in the sham surgery group(P>0.05).CONCLUSION:The excitability of PVN is increased during the asthmatic attack.PVN plays a key role in the regulation of asthma.Both electrolytic and KA lesions of PVN can significantly relieve the asthmatic symptoms of rats,and improve their lung function.

Fos expression incatecholaminergic medullary neu-rons induced by chemical stimulation of stomach projecting to the paraventricular nucleus of hypothalamus in rats

AIM To determine whether medullary catecholaminergic neurons expressing Fos induced by chemical stimulation of the stomach project to the paraventricular nucleus of hypothalamus (PVH) in rats. METHODS A triple labeling method of horseradish peroxidase (HRP) retrograde tracing combined with Fos (ABC method) and tyrosin hydroxylase (TH) (PAP method) immunohistochemical stainings was used in the present study. RESULTS Seven kinds of labeled neurons were found in the nucleus tractus solitarii (NTS), the ventrolateral medulla (VLM) and the reticular formation of the medulla (RF): Fos like immunoreactive (LI) neurons, TH LI neurons and HRP retrogradely single labeled neurons, Fos/HRP, Fos/TH and HRP/TH double labeled neurons, and Fos/HRP/TH triple labeled neurons. CONCLUSION Ascending projections from the NTS, VLM and RF to the PVH might be involved in the transmitting process of the visceral noxious stimulation.

Reactive oxygen species in paraventricular nucleus involved in cardiac sympathetic afferent reflex in rats

Objective： The present study was designed to determine if reactive oxygen species （ROS） in the paraventricular nucleus （PVN） were involved in modulating cardiac sympathetic afferent reflex （CSAR） in anesthetized rats. Methods： Malondialdehyde （MDA）, the end product of lipid peroxidation, in the PVN, was determined by thiobarbituric acid （TBA） spectrometric method. Renal sympathetic nerve activity （RSNA） and arterial pressure were recorded in sinoaortic-denervated and cervical-vagotomized rats. The CSAR was evaluated by the response of the RSNA evoked by epicardial application of bradykinin （BK, 0.4 9g）. Results： The MDA in the PVN was significantly increased after epicardial application of BK compared with control （2.0 ±0.3 vs 0.8 ±0.1 nmol/mg protein, P 〈 0.01）. Microinjection of a superoxide anion scavenger, tiron （20 nmol） into the PVN significantly inhibited the CSAR evoked by BK （12.3±1.9 vs4.2± 1.2%, P 〈0.01） and decreased MDA level （1.9±0.3 vs 0.6 ±0.1 nmol/mg protein, P 〈0.01） compared with control. Conclusion： The ROS in the PVN is involved in modulating the CSAR in rats.

Distribution of peptidergic neurons in the hypothalamic paraventricular nucleus of the rat

Distribution of peptidergic neurons in the hypothalamic paraventricular nucleus(PVN)of the rat was investigated by means of immunohistochemical technique,and thearea,perimeter,maximum diameter,minimum diameter and grey scale of peptidergicneuronal cell bodies were measured with an image analyser.All of these peptidergicneurons,oxytocin(OXY)-,vasopressin(VP)-,substance P(SP)-,corticotropin releasingfactor(CRF)-,thyrotropin releasing hormone(TRH)-,neurotensin(NT)-,cholecystokinin(CCK)-,somatostatin(SOM)-,galanin(GAL)-,leucine-enkephalin(L-ENK)-,vasoactive intestine polypeptide(VIP)-,and ACTH-like neurons,were ob-served in the PVN.The data of image analysis showed that the area of peptidergicneuronal cell bodies in the magnocellular subnucleus part of the PVN was similar,but wasdifferent in the parvocellular subnucleus part of the PVN.

Inhibitory effects of ketamine and L--NAME on expression of c-fos and NOS in hypothalamic paraventricular nucleus after acute hypothermia and hypoxia in rats

Objective: To determine whether NMDA receptor activation mediates the expression of c--fos and NOS and study the relationship between the expression of c--fos and NOS in the hypothalamic paraventricularnucleus (PVN) following acute hypothermia and hypoxia. Methods: Fos immunohistochemistry, NADPH--d histochemistry and Fos/NADH--d double labeling were used. Results: Acute hypothermia and hypoxia induced the overexpression of on fos and NOS in PVN in rats. Pretreatment with ketamine, a NMDA receptor antagonist, resulted in partial inhibition of the expression of c--fos and NOS and that with blocker of NOS resulted in significant inhibition of the expression of c--fos. Conclusion: The activation of NMDA receptor is involved in the expression of c- fos and NOS in PVN in the rats subjected to acute hypothermia and hypoxia.Meanwhile, hypothalamic endogenous NO participates in adaptive reaction to hypothermia and hypoxia,which might be related to the modulation of c- fos expression.

室旁核H_(2)S对高盐性高血压大鼠内质网应激蛋白GRP78的影响

目的:通过外源给予高盐性高血压大鼠室旁核(paraventricular nucleus,PVN)硫化氢(hydrogen sulfide,H 2S)供体GYY4137,观察PVN中GRP78的蛋白表达含量变化,探讨室旁核H 2S对高盐性高血压GRP78的影响。方法:雄性Dahl盐敏感大鼠40只,随机分成4组,即正常对照组、正常给药组、模型组和模型给药组。分别饲喂正常盐饲料(0.3%NaCl)和高盐饲料(8%NaCl)4周后,双侧PVN插管持续微量注射GYY4137,采用尾动脉无创测量平均动脉压(mean arterial pressure,MAP),ELISA法检测血浆去甲肾上腺素(norepinephrine,NE),采用免疫组织化学技术及Western blotting法检测PVN中GRP78蛋白表达。结果:(1)与正常对照组相比,高盐模型组的MAP、血浆NE水平明显升高(P<0.01);与高盐模型组相比,高盐干预组MAP、血浆NE水平明显下降(P<0.01);(2)与正常对照组相比,高盐模型组室旁核中GRP78的蛋白表达明显升高(P<0.01);与高盐模型组相比,高盐干预组室旁核中GRP78的蛋白表达明显下降(P<0.01)。结论:室旁核H 2S可通过降低外周交感神经活动改善高盐性高血压,其机制可能与抑制室旁核内质网应激有关。

糖尿病诱导的小鼠室旁核催产素和加压素阳性神经元FOS表达

目的:探索糖尿病(DM)不同状态下小鼠下丘脑室旁核(PVN)催产素和加压素阳性神经元的FOS表达变化。方法:腹腔注射溶媒或链脲佐菌素(STZ)制备对照组或糖尿病小鼠模型,根据机械痛测试区分糖尿病痛(DNP组)与非痛组(DWP组)。采用免疫组化和免疫荧光染色技术检测PVN内FOS、催产素(OXT)和加压素(VP)阳性神经元的分布及双标情况,并进行计数和比较。结果:7 d时三组(Control组、DNP组和DWP组)小鼠PVN内均有较多的FOS表达,而28 d时DWP和DNP组FOS的表达几近于无,与7 d组相比差异显著(P<0.05或0.001)。与对照组相比,DNP组和DWP组动物的VP和OXT荧光染色同样存在随着造模时间延长染色强度减弱的趋势(P<0.05)。VP、OXT与FOS的双标染色计数结果显示,在DWP 7 d组,VP/FOS双标细胞数为74.33±22.10,占VP阳性细胞数的(56.64±7.52)%,而OXT/FOS的双标率则仅为(10.44±3.14)%。在DNP 7 d组,OXT/FOS双标细胞数为51.00±31.80,占OXT阳性细胞数的(18.50±9.51)%,而VP/FOS的双标率仅为(9.34±3.27)%。与此相对,28 d组FOS的表达锐减,几乎无双标细胞。结论:下丘脑PVN内的VP和OXT阳性神经元在糖尿病痛与非痛,疾病发展的不同阶段存在明显不同的可塑性变化特点,理解这些变化对于揭示糖尿病及其并发症的神经机制具有重要意义。

Glutamatergic neurons in the paraventricular nucleus of the hypothalamus participate in the regulation of visceral pain induced by pancreatic cancer in mice

Background:Visceral pain induced by pancreatic cancer seriously affects patients’quality of life,and there is no effective treatment,because the mechanism of its neural circuit is unknown.Therefore,the aim of this study is to explore the main neural circuit mechanism regulating visceral pain induced by pancreatic cancer in mice.Methods:The mouse model of pancreatic cancer visceral pain was established on C57BL/6N mice by pancreatic injection of mPAKPC-luc cells.Abdominal mechanical hyperalgesia and hunch score were performed to assess visceral pain;the pseudorabies virus(PRV)was used to identify the brain regions innervating the pancreas;the c-fos co-labeling method was used to ascertain the types of activated neurons;in vitro electrophysiological patch-clamp technique was used to record the electrophysiological activity of specific neurons;the calcium imaging technique was used to determine the calcium activity of specific neurons;specific neuron destruction and chemogenetics methods were used to explore whether specific neurons were involved in visceral pain induced by pancreatic cancer.Results:The PRV injected into the pancreas was detected in the paraventricular nucleus of the hypothalamus(PVN).Immunofluorescence staining showed that the majority of c-fos were co-labeled with glutamatergic neurons in the PVN.In vitro electrophysiological results showed that the firing frequency of glutamatergic neurons in the PVN was increased.The calcium imaging results showed that the calcium activity of glutamatergic neurons in the PVN was enhanced.Both specific destruction of glutamatergic neurons and chemogenetics inhibition of glutamatergic neurons in the PVN alleviated visceral pain induced by pancreatic cancer.Conclusions:Glutamatergic neurons in the PVN participate in the regulation of visceral pain induced by pancreatic cancer in mice,providing new insights for the discovery of effective targets for the treatment of pancreatic cancer visceral pain.

PVN和脑刺激镇痛关系初探

用４％水合氯醛麻醉大鼠，在下丘脑室旁核（ＰＶＮ）、中脑导水管周围灰质（ＰＡＧ）埋藏双极刺激电极或不锈钢管，以便刺激、损毁或电泳药物，并暴露脊髓背角，利用微电极记录脊髓背角神经元对伤害刺激坐骨神经单位反应。实验观察到：（１）电刺激ＰＶＮ或注射盐酸吗啡可使大鼠痛阈显著升高。微量注射纳络酮可翻转盐酸吗啡的作用，（２）电刺激ＰＶＮ可抑制脊髓背角神经元伤害反应，其作用持续２０ｍｉｎ，在刺激后３ｍｉｎ作用最显著。（３）电解损毁ＰＡＧ后，刺激ＰＶＮ抑制脊髓背角神经元伤害反应仍然存在。实验结果表明：ＰＶＮ是脑内镇痛的主要核团之一，其作用通过ＰＡＧ实现，也可通过ＰＶＮ—脊髓背角直接投射的途径。

刺激大鼠 PVN 影响痛感受下行途径的研究

在大鼠腰脊髓背角泳入辣根过氧化酶（ＨＲＰ），下丘脑室旁核（ＰＶＮ）找到逆行标记细胞；在ＰＶＮ泳入ＨＲＰ，脊髓内均有顺行标记纤维和终末分布于脊髓背角第Ⅰ、Ⅱ、和Ⅳ、Ⅴ板层。可见大鼠ＰＶＮ－脊髓背角间存在直接纤维联系。用行为测痛法观察到电刺激ＰＶＮ或注射谷氨酸钠、盐酸吗啡，痛阈均显著升高。纳络酮可翻转盐酸吗啡的作用。电刺激ＰＶＮ的同时，电针双侧“足三里”痛阈升高更显著，说明刺激ＰＶＮ可使痛阈升高，电针“足三里”有协同作用。用微电极记录脊髓背角神经元伤害单位活动，其反应可被电刺激ＰＶＮ所抑制。分别电解中脑导水管周围灰质（ＰＡＧ）和中缝大核（ＮＲＭ）后，ＰＶＮ对脊髓背角神经元伤害反应的抑制仍存在。实验结果表明，ＰＶＮ参与了痛觉下行的调制过程。

淫羊藿苷对去卵巢大鼠骨和下丘脑不同核团ERβ mRNA表达的影响

目的观察淫羊藿苷对去卵巢大鼠骨和下丘脑不同核团ERβmRNA表达的影响,探讨其治疗绝经后骨质疏松的作用机制。方法将10～11月龄SD♀大鼠60只,随机分为假手术组、去卵巢模型组、淫羊藿苷小、中、大剂量组(每组12只)。以双侧卵巢切除法建立大鼠骨质疏松模型。分别用淫羊藿苷小、中、大剂量给药4个月,采用RT-PCR法,观察各组大鼠骨和下丘脑室旁核、视上核、弓状核ERβmRNA表达的变化。结果大鼠卵巢切除后,血清E2水平、椎骨骨密度、子宫湿重、胫骨和下丘脑弓状核ERβmRNA表达明显降低(P<0.01),下丘脑室旁核、视上核ERβmRNA表达均明显升高(P<0.01)。与去卵巢模型组比较,淫羊藿苷50.0和100.0 mg.kg-1组治疗后,血清E2水平、椎骨骨密度、胫骨和下丘脑弓状核ERβmRNA表达明显升高(P<0.01),下丘脑室旁核、视上核ERβmRNA表达均明显降低(P<0.01),子宫湿重无明显改变(P>0.05)。结论淫羊藿苷可以改善切除卵巢所致的骨质疏松大鼠的骨密度,对子宫无不良反应。其机制可能与其选择性调节去卵巢骨质疏松大鼠下丘脑不同核团ERβmRNA表达水平有关,调节下丘脑功能活动是其途径之一。

刺激室旁核及加压素对大鼠胃缺血-再灌注损伤的保护作用

采用夹闭大鼠腹腔动脉 30min ,松开动脉夹血流复灌 1h的胃缺血 再灌注损伤 (gastricischemia reperfu sioninjury ,GI RI)模型 ,观察了电或化学刺激室旁核 (paraventricularnucleus,PVN)及外源性加压素 (arginine vasopres sion ,AVP)对GI RI的影响 ,并对PVN的调控通路进行了初步分析。结果表明 :电或化学刺激PVN后 ,GI RI显著减轻 ;损毁双侧孤束核 (nucleustractussolitarius,NTS)或一侧NTS内注射AVP V1受体阻断剂 ,均能取消电刺激PVN对GI RI的效应 ;去除脑垂体后不影响PVN的作用 ;切断膈下迷走神经或切除腹腔交感神经节 ,则能加强电刺激PVN对GI RI的影响 ;PVN内注射不同剂量的AVP同样能减轻大鼠GI RI损伤。结果提示 :PVN及AVP对大鼠GI RI具有保护作用 ;PVN的这种作用可能是因电或化学刺激后 ,激活了其中的加压素能神经元 ,经其下行投射纤维释放AVP作用于NTS神经元的AVP V1受体 ,并通过迷走和交感神经介导 ,从而影响GI RI;而似与PVN

胃缺血/再灌注损伤引起大鼠脑室旁核及孤束核c-fos表达

目的 :观察电和化学刺激下丘脑室旁核 (PVN)对大鼠胃缺血 /再灌注损伤 (GI/RI)的影响及孤束核 (NTS)在其中的作用和GI RI后PVN、NTS内c fos表达的情况。方法 :夹闭大鼠腹腔动脉 30min ,松开动脉夹血流复灌 1h制备GI/RI模型 ,应用Fos免疫组织化学法 (ABC法 )观察GI RI后中枢神经系统内c fos表达的情况。结果 :①电和化学刺激PVN后 ,GI/RI减轻。②损毁双侧NTS后 ,能取消电刺激PVN对GI RI的影响。③GI RI能引起PVN、NTS等核团内c fos表达增加。结论 :GI RI的伤害性刺激影响了PVN、NTS的功能。PVN、NTS参与了对GI RI的调控。

电刺激室旁核对大鼠应激性胃粘膜损伤的影响

电刺激室旁核(PVN)有加重大鼠应激性胃粘膜损伤的作用;PVN内微量注射神经元胞体兴奋剂L-谷氨酸钠和电刺激PVN的效应相同;电解损毁双侧PVN或对其电刺激后,使应激性胃粘膜损伤明显减轻,切断膈下迷走神经或皮下注射阿托品后,可显著减轻电刺激PVN加重大鼠应激性胃粘膜损伤的效应;电刺激PVN使胃粘膜血流量减少,但对胃液量、胃酸排出量、胃蛋白酶活性及胃壁结合粘液量均无显著影响。从而表明,PVN是影响应激性胃粘膜损伤的特异性中枢部位之一,当其兴奋时,可加重应激性胃粘膜损伤,并可能是通过迷走神经胆碱能纤维起作用的,且与胃粘膜血流量的减少有关;电刺激PVN加重胃粘膜损伤似不是由胃液量、胃酸、胃蛋白酶活性及胃壁结合粘液量等因素的改变引起的。

电刺激大鼠下丘脑室旁核对胃缺血-再灌注损伤的影响

采用夹闭大鼠腹腔动脉 30min ,松开动脉夹血流复灌 1h的胃缺血 再灌注损伤模型 ,观察了电刺激和电损毁下丘脑室旁核 (paraventricularnucleus,PVN)对大鼠胃缺血 再灌注损伤 (gastricischemia reperfusioninjury ,GI RI)的影响 ,并对其作用机制进行了初步探讨。结果表明 :电刺激PVN后GI RI显著减轻 ,且有强度 效应依赖关系 ;PVN内注射胞体兴奋剂L 谷氨酸后 ,与电刺激PVN的效应相同 ;电解损毁双侧PVN则能加重GI RI;电刺激PVN能显著降低GI RI大鼠的胃粘膜丙二醛 (MDA)含量及胃液酸度和胃蛋白酶活性 ,但对其超氧化物歧化酶 (SOD)的活性及胃液量、总酸排出量、胃壁结合粘液量无显著影响。提示PVN对GI RI具有保护作用 ,其作用机制可能与降低GI RI大鼠的胃粘膜MDA含量、胃蛋白酶活性、胃液酸度有关 ,而与胃液量、总酸排出量、胃壁结合粘液量等因素无明显关系。

烫伤大鼠室旁核和触液神经元中胆囊收缩素的变化

目的明确胆囊收缩素在烫伤应激中的确切作用。方法在大鼠清醒状态下给予标准的２５％Ⅲ度皮肤烫伤，伤后２４ｈ杀动物，用免疫细胞化学ＡＢＣ法显示ＰＶＮ和ＣＳＦ－ＣＮｓ的ＣＣＫ阳性神经元，结果用显微图像分析技术处理。结果（１）烫伤大鼠ＰＶＮ代表平面ＣＣＫ神经元的总面积增大，免疫染色无明显变化。（２）正中隆起（ｍｅｄｉｎｅｍｉｎｅｎｃｅ，ＭＥ）的ＣＣＫ免疫染色阳性纤维的面积密度无显著性差异而免疫染色减弱。（３）烫伤大鼠第三脑室室管膜内ＣＣＫ免疫染色阳性的ＣＳＦ－ＣＮｓ数量、面积和免疫染色强度均高于对照组。结论烫伤应激使ＣＣＫ在胞体的合成和末梢的释放均增加。烫伤后大量ＣＳＦ－ＣＮｓ的出现为ＣＣＫ释放入脑脊液提供了一条新的途径。

力竭运动对大鼠室旁核和视上核神经元一氧化氮合酶表达的影响

目的:研究下丘脑室旁核(PVN)和视上核(SON)中神经元型一氧化氮合酶(nNOS)与运动性疲劳的关系。方法:雄性成年大鼠32只随机分为对照组、运动后即刻组、运动后0.5h组和运动后4h组。实验组强迫游泳致力竭制成运动性疲劳模型,用ABC免疫组织化学方法观测室旁核和视上核nNOS表达状况,并进行半定量分析和统计学处理。结果:运动后即刻,室旁核和视上核nNOS的表达均明显低于对照组(P<0.001;P<0.05);运动后0.5h,nNOS的表达均比对照组低(P<0.001);运动后4h,室旁核nNOS的表达与对照组无显著差异,而视上核nNOS的表达与对照组相比仍明显降低(P<0.05)。结论:运动性疲劳使大鼠下丘脑室旁核和视上核nNOS的表达降低,提示室旁核和视上核nNOS与中枢运动性疲劳的形成密切相关,它们可能在机体对运动性疲劳的反应中起调节作用。

甲基强的松龙对脊髓损伤后下丘脑室旁核FOS和NOS表达的影响

目的:观察甲基强的松龙(methylprednisolone,MP)对急性脊髓损伤后下丘脑室旁核(paraventricular nucleus,PVN)神经元FOS和一氧化氮合酶(nitric oxide synthase,NOS)表达的影响。方法:将大鼠分为对照组、脊髓损伤组、MP治疗组。脊髓损伤组在第4胸髓节段横断;治疗组在脊髓横断后每天给予1次静脉注射甲基强的松龙(30 mg/kg),分别持续1天、1周或4周。NADPH-d组织化学及FOS免疫组织化学方法观察各组PVN内FOS与NOS表达情况。结果:与对照组相比,脊髓损伤组PVN内FOS、NOS表达显著增高。MP治疗1周和4周PVN内FOS、NOS表达较损伤组显著下降(P<0.01)。结论:甲基强的松龙可能对脊髓损伤后PVN内神经元继发性损伤有一定保护作用。