首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 140 毫秒
1.
NO对大鼠睡眠-觉醒的调节   总被引:10,自引:0,他引:10  
目的和方法:通过对大鼠侧脑室微量注射NOS抑制剂L-NAME及NO的前体L-精氨酸(L-Arg)观察两种物质对大鼠睡眠-觉醒的影响。结果:注射1mg L-NAME(5μL)后4h觉醒(W)明显增加,尤以注射后第1 ̄2h显著;4h慢波睡眠(SWS)明显减少,该效应同样以注射后第1 ̄2h显著;异相睡眠(PS)无明显变化。小剂量L-NAME(0.2mg,5μl)对大鼠的W、SWS、PS无明显影响;同样方  相似文献   

2.
L-NNA及NO供体对延髓腹外侧头端区神经元自发放电的影响   总被引:3,自引:1,他引:2  
在麻醉大鼠观察了静注NO合成酶抑制剂N-硝基左旋精氨酸(L-NNA)和NO供体──硝普钠(SNP)和SIN-I对血压、心率和延髓腹外侧头端区(RVLM)神经元自发放电活动的影响,旨在探讨L-arg:NO通路对动脉血压调节的中枢作用部位。所得结果如下:(1)静注L-NNA后,平均动脉压(MAP)升高,心率(HR)加快,11个RVLM神经元自发放电频率增加。这些变化发生于给药后5min,持续时间达30min以上。(2)静注SNP后,MAP降低,HR加快,23个RVLM神经元自发放电频率降低,且有剂量依赖性。SNP作用发生快,持续时间短。为了排除脑缺血的影响,还特意向一侧颈动脉内注射相同剂量SNP,结果引起MAP轻度降低,而HR无明显改变,但RVLM神经元自发放电频率仍显著降低。(3)静注另一NO供体SIN-I后,MAP降低,11个RVLM神经元自发放电频率降低.与SNP的效应基本一致。以上结果提示,RVLM是L-arg:NO通路实现动脉血压调节的一个中枢作用部位。  相似文献   

3.
褪黑素对大鼠中脑导水管周围灰质内阿片肽释放的影响   总被引:4,自引:0,他引:4  
Yu CX  Wu GC  Xu SF  Chen CH 《生理学报》2000,52(3):207-210
本文采用推挽灌流技术、放射免疫测定法,观察褪黑素(melatonin,MEL)对大鼠中脑导水管周围灰质(PAG)推挽灌流液中β-内啡肽(β-Ep)、亮氨酸脑啡肽(L-EK)含量的影响,以探讨MEL镇痛效应的中枢机制。结果显示,给药组大鼠腹腔注射(ip)MEL110mg/kg后30-50min,PAG灌流液中β-Ep含量显著增加,而L-EK含量未见显著变化;在推挽灌流同时用50℃热水刺激甩尾法测定痛  相似文献   

4.
Xue BJ  Wang ZA  He RR  Ho SY 《生理学报》1998,50(1):55-60
用细胞外记录单位放电技术,在大鼠海马脑片上观察了L-精氨酸(L-arg)、N-硝基L-精氨酸(L-NNA)及SIN-1对谷氨酸(glutamate,Glu)诱导的CA1区神经元放电的影响。旨在了解L-精氨酸:NO通路在谷氨酸诱发的海马放电中的作用及其可能的机制。结果如下:(1)用GlU(0.5mmol/L)灌流海马脑片1min,12个放电单位放电频率明显增加,表现为癫痫样放电;(2)海马脑片2mi  相似文献   

5.
冯康  郭学勤 《生理学报》1997,49(5):491-496
雄性Sprague-Dawley大鼠,用乌拉坦(700mg/kg)和氯醛糖(30mg/kg)腹腔麻醉。在双侧头端延髓腹外侧区(rVLM区)每侧微量注射血管加压素(AVP)(10pmol/0.1μl)可引起平均动脉压(MBP)升高,心率(HR)变化不明显,每侧微量注射AVP的V1受体拮抗剂d(CH2)5[Tyr(Me)^2]AVP(0.1nmol/0.1μl)后MBP和HR无明显变化。若预先在rVL  相似文献   

6.
在麻醉大鼠观察了向延髓腹外侧区微量注射NO合成酶抑制剂N-硝基左旋精氨酸(LNNA)和硝普钢(SNP)对血压、心率和肾交感神经活动的影响,旨在探讨中枢左旋精氨酸-NO通路在动脉血压调节中的作用及其机制。实验结果如下:(1)向延髓腹外侧头端区(RVLM)注射L-NNA后,平均动脉压(MAP)升高,肾交感神经活动(RSNA)增强;心率(HR)减慢,但无统计学意义。MAP和RSNA的变化持续30min以上;此效应可被预先静注左旋精氨酸所逆转。(2)向RVLM微量注射SNP,MAP降低,RSNA减弱;但HR的变化无统计学意义。(3)向延髓腹外侧尾端区(CVLM)注射L-NNA,MAP降低,HR减慢,RSNA减弱。(4)向CVLM微量注射SNP,MAP升高,RSNA增强,而心率无明显变化。以上结果表明,中枢左旋精氨酸-NO通路对延髓腹外侧部的神经元活动有调变作用。  相似文献   

7.
胍基丁胺对大鼠血流动力学的影响及其细胞机制   总被引:8,自引:5,他引:3  
Li XT  He RR 《生理学报》1999,(2):229-233
在麻醉大鼠研究静注胍基丁胺(AGM)对血流动力学的影响,并初步探讨其机制。结果如下:(1)静注AGM(10mg/kg)后,HR,MAP,LVP,±LVdp/dtmax,CI和TPRI均明显下降;(2)预先静注NOS抑制剂LNNA(15mg/kg)或腹腔内注射鸟苷酸环化酶抑制剂亚甲基蓝(50mg/kg),均不能阻断AGM的降压作用;(3)预先静注咪唑啉受体和α2肾上腺素能受体阻断剂idazoxan(2mg/kg)则可明显阻抑AGM的降压效应。以上结果表明,AGM对麻醉大鼠的降压机制,在于显著抑制心肌收缩性而使心输出量降低,以及舒张外周血管致使总外周阻力下降;此效应似主要由IR和/或α2AR所介导。  相似文献   

8.
我们以往的工作证实成年自发高血压大鼠(SHR与SHRsp)肠系膜动脉由乙酰胆碱引起的内皮依赖性舒张(EDR)减弱。为进一步探讨EDR减弱的机制,本文观察了一氧化氮(NO)合成酶抑制剂左旋硝基精氨酸(L-NNA)及EDRF灭活剂还原型血红蛋白(RHb)对卒中易感型自发高血压大鼠(SHRsp)与常压对照(WKY)大鼠肠系膜动脉ACh内皮依赖性舒张(EDR)的影响。发现L-NNA(10(-3)mol/L)可使SHRsp弱于WKY的AChEDR(10(-8)-10(-5)mol/L)的差异消失,RHb(10(-5)mol/L)则仅在10(-7)-10(-8)mol/LACh时使SHR(sp)肠系膜动脉EDR弱于WKY的差异消失。将WKY在加入L-NNA后的与加入RHb后的ACh(10(-8)-10(-5)mol/L)EDR进行比较,无显著差异。而将SHRsp在L-NNA后的与RHb后的ACh(10(-8)-10(-6)mol/L)EDR进行比较,则有显著差异。并且,SHRsp的有内皮肠系膜动脉条对RHb的敏感性与WKY接近,对L-NNA的敏感性则低于WKY。表明高血压时肠系膜动脉内皮依赖性舒张减弱中,EDRF机制与  相似文献   

9.
百脉根愈伤组织原生质体再生植株   总被引:1,自引:0,他引:1  
百脉根无菌苗幼茎在含2.0mg/L-,2,4-D,0.1mg/L2-ip的MS培养基上诱导和继代培养愈伤组织。选取绿色松散颗粒愈伤组织分离原生质体。原生质体培养在调整珠KM8P,V-KM,MS和SH培养基上「含300mg/L,CH,2%CW,2%蔗糖,6%葡萄糖,2.0mg/L,2,4-D,0.5mgg/L,BA,5mmol/L MES」,原生质体再生细胞均能分裂,并形成小愈伤组织,但以KM80为  相似文献   

10.
EDRF对PE引起的大鼠主动脉缩血管效应的作用   总被引:1,自引:0,他引:1  
本文研究EDRF(endothelium-derivedrelaxingfactor,EDRF)对PE(phenylephrine)引起的大鼠主动脉收缩反应的影响。内皮完整和去内皮的大鼠主动脉环悬挂于器官浴槽中,测定血管的张力和收缩速度的变化。所有的实验在消炎痛(indomethacin,10μmol/L)存在下进行。用美兰(methyleneblue,MB,10μmol/L)或左旋硝基精氨酸(NG-nitro-L-arginine,L-NNA,30μmol/L)处理内皮完整的大鼠主动脉环,PE的剂量-收缩张力曲线明显左移,EC30值均降低5倍,最大反应比率分别为1.6±0.4和1.6±0.5。在去内皮的大鼠主动脉环中,经MB和L-NNA处理后,仍可见EC30下降3倍,最大反应比率均为1.0±0.2。后者可能与血管平滑肌产生少量EDRF有关。我们的结果提示PE对血管的收缩反应也受血管内皮和平滑肌产生的EDRF的调控  相似文献   

11.
《Life sciences》1996,58(6):PL103-PL110
The effects of the central (CB1) cannabinoid receptor antagonist SR 141716A on the sleep-waking cycle were investigated in freely-moving rats using time scoring and power spectral analysis of the electroencephalogram (EEG). Over a 4-hour recording period, SR 141716A (0.1, 0.3, 1, 3 and 10 mg/kg I.P.) dose-dependently increased the time spent in wakefulness at the expense of slow-wave sleep (SWS) and rapid eye movement sleep (REMS), delayed the occurrence of REMS but did not change the mean duration of REMS episodes. Moreover, the compound induced no change in motor behavior. At the efficient dose of 3 mg/kg I.P., SR 141716A reduced the spectral power of the EEG signals typical of SWS but did not affect those of wakefulness. Taken together, these results demonstrate that the EEG effects of SR 141716A reflect arousal-enhancing properties. In addition, the present study suggests that an endogenous cannabinoid-like system is involved in the control of the sleep-waking cycle.  相似文献   

12.
REM sleep rebound is a common behavioural response to some stressors and represents an adaptive coping strategy. Animals submitted to multiple, intermittent, footshock stress (FS) sessions during 96 h of REM sleep deprivation (REMSD) display increased REM sleep rebound (when compared to the only REMSD ones, without FS), which is correlated to high plasma prolactin levels. To investigate whether brain prolactin plays a role in stress-induced REM sleep rebound two experiments were carried out. In experiment 1, rats were either not sleep-deprived (NSD) or submitted to 96 h of REMSD associated or not to FS and brains were evaluated for PRL immunoreactivity (PRL-ir) and determination of PRL concentrations in the lateral hypothalamus and dorsal raphe nucleus. In experiment 2, rats were implanted with cannulas in the dorsal raphe nucleus for prolactin infusion and were sleep-recorded. REMSD associated with FS increased PRL-ir and content in the lateral hypothalamus and all manipulations increased prolactin content in the dorsal raphe nucleus compared to the NSD group. Prolactin infusion in the dorsal raphe nucleus increased the time and length of REM sleep episodes 3 h after the infusion until the end of the light phase of the day cycle. Based on these results we concluded that brain prolactin is a major mediator of stress-induced REMS. The effect of PRL infusion in the dorsal raphe nucleus is discussed in light of the existence of a bidirectional relationship between this hormone and serotonin as regulators of stress-induced REM sleep rebound.  相似文献   

13.
Pressor effect of NG-nitro-L-arginine in pentobarbital-anesthetized rats   总被引:4,自引:0,他引:4  
Y X Wang  C C Pang 《Life sciences》1990,47(24):2217-2224
The pressor effect of NG-nitro-L-arginine (L-NNA), a potent inhibitor of nitric oxide (NO) synthesis, was studied in pentobarbital anesthetized rats. Iv injections of L-NNA from 0.25 to 8 mg/kg caused bradycardia and a dose-dependent increase in mean arterial pressure (MAP) with a maximal response of 43 +/- 5 mmHg and ED50 value of 1.3 +/- 0.2 mg/kg. The time course of the response to the injection of a single dose of L-NNA was also determined. Peak response was reached 60 min after the injection of a single dose (4 mg/kg, iv) and the effect lasted greater than 5 h. The rising phase of the pressor response was accompanied by slight bradycardia while the recovery phase was associated with significant tachycardia. Iv injections of L-arginine (12.5-200 mg/kg) caused transient dose-dependent reductions in MAP. The pressor effect of L-NNA (4 mg/kg, iv bolus) was dose-dependently attenuated by L-arginine. The results show that L-NNA is an efficacious and long-acting pressor agent and are consistent with the hypothesis that endogenous NO plays an important role in the regulation of blood pressure.  相似文献   

14.
研究大鼠在福尔马林诱发胃伤害性刺激时脑干内星形胶质细胞及神经元的变化。应用免疫组织化学三重标记法在脑原位切片同时显示脑干内Fos蛋白,胶质原纤维酸性蛋白(GFAP),酪氨酸羟化酶(TH)的表达,结果显示:1、在福尔马林诱发胃伤害性刺激后,脑干胶质细胞GFAP表达阳性,并表现出明显的核团或亚核定位特点,在延髓内脏带(MVZ0,中缝大核(RMg),蓝斑(LC),臂旁外侧核(LPB),中缝背核(DR),中脑导水管周围灰质腹外侧区(vlPAG),上丘中灰层(IngSC)等脑区有较多的Fos阳性细胞,而且Fos阳性表达的分布与上述GFAP阳性分布基本一致;2、MVZ,LC,DR,vlPAG等部位有大量Fos及TH双标阳性神经元,周围有密集的GFAP阳性细胞;3、随着刺激后存活时间的变化,GFAP与Fos阳性细胞的反应均经历逐渐升高后又渐降低直至消失的变化。结果表明:上述核团的神经元和星形胶质细胞可能同时参与了内脏痛及其调节过程。  相似文献   

15.
基底外侧杏仁核对睡眠-觉醒的调节作用   总被引:13,自引:0,他引:13  
Zhu GQ  Zhong MK  Zhang JX  Zhao LZ  Ke DP  Wang M  Shi L 《生理学报》1998,50(6):688-692
采用多道睡眠描记方法,观察了基底外侧杏仁核在睡眠-觉醒调节中的作用。结果发现,电损毁双侧BLN引起慢波睡眠和快波睡眠增加,觉醒减少;在双侧BLN内注射选择性损毁神经元胸体剂量的红藻氨酸引起双相效应,注射KA后第1天出现失眠,自第3天开始,SWS增多,W减少,但PS无显著变化。  相似文献   

16.
Electroacupuncture (EAc) possesses a broad therapeutic effect, including improvement of sleep disturbances. The mechanism of sleep improvement with EAc, however, is still unclear. The present study investigated the effects of EAc stimulation of Anmian (extra) acupoints on sleep organization and the implication of an active structure, the caudal nucleus tractus solitarius (NTS). Rats were implanted with electroencephalogram (EEG) recording electrodes, and 32-gauge acupuncture needles were bilaterally inserted into Anmian (extra) acupoints in the rats, followed by electrical stimulation for 20 min. Twenty-three-hour continuous EEGs were then recorded. Results showed that rapid eye movement sleep (REMS) was enhanced during the dark period when a single EAc stimulation was given 25 min prior to the onset of the dark period. REMS and slow-wave sleep (SWS) increased during the dark period after administration of EAc stimuli on 2 consecutive days. Electrical stimulation of non-acupoints produced no change in the sleep pattern. Pharmacological blockade of muscarinic cholinergic receptors by systemic administration of scopolamine dose-dependently attenuated EAc-induced changes in REMS and SWS. Furthermore, electrical lesions in the bilateral caudal NTS produced significant blockade of EAc-induced sleep enhancement. However, in rats without EAc, scopolamine increased SWS during the dark period, but caudal NTS lesions did not alter sleep. In addition, neither EAc nor scopolamine with EAc manipulation produced any change in the slow-wave activity (SWA) during SWS; however, the SWA during SWS was significantly reduced after caudal NTS lesion with EAc. These results suggest that the caudal NTS may be involved in the regulation of EAc-induced sleep alterations.  相似文献   

17.

Background

Oleoylethanolamide (OEA) and palmitoylethanolamide (PEA) are amides of fatty acids and ethanolamine named N-acylethanolamines or acylethanolamides. The hydrolysis of OEA and PEA is catalyzed by the fatty acid amide hydrolase (FAAH). A number of FAAH inhibitors that increase the levels of OEA and PEA in the brain have been developed, including URB597. In the present report, we examined whether URB597, OEA or PEA injected into wake-related brain areas, such as lateral hypothalamus (LH) or dorsal raphe nuclei (DRN) would promote wakefulness (W) in rats.

Methodology and Principal Findings

Male Wistar rats (250–300 g) were implanted for sleep studies with electrodes to record the electroencephalogram and electromyogram as well as a cannulae aimed either into LH or into DRN. Sleep stages were scored to determine W, slow wave sleep (SWS) and rapid eye movement sleep (REMS). Power spectra bands underly neurophysiological mechanisms of the sleep-wake cycle and provide information about quality rather than quantity of sleep, thus fast Fourier transformation analysis was collected after the pharmacological trials for alpha (for W; α = 8–12 Hz), delta (for SWS; δ = 0.5–4.0 Hz) and theta (for REMS; θ = 6.0–12.0 Hz). Finally, microdialysis samples were collected from a cannula placed into the nucleus accumbens (AcbC) and the levels of dopamine (DA) were determined by HPLC means after the injection of URB597, OEA or PEA. We found that microinjection of compounds (10, 20, 30 µg/1 µL; each) into LH or DRN during the lights-on period increased W and decreased SWS as well as REMS and enhanced DA extracellular levels.

Conclusions

URB597, OEA or PEA promoted waking and enhanced DA if injected into LH or DRN. The wake-promoting effects of these compounds could be linked with the enhancement in levels of DA and indirectly mediated by anandamide.  相似文献   

18.
实验采用 NADPH组织化学和 5 - HT免疫组织化学双重显色方法研究了 5 - HT和一氧化氮合酶在大鼠中脑导水管周围灰质 (PAG)和中缝核簇神经元的分布特征及共存情况。结果表明 ;(1 )在 PAG腹外侧区中观察到大量的 NOS阳性神经元和 5 - HT样免疫阳性神经元 ,但是 NOS/ 5 - HT双标神经元较少 ,仅占该区 5 - HT样免疫阳性神经元 2 0 .1 % ,并且主要分布在该区的内侧部 ;在 PAG的背外侧区中观察到密集的 NOS阳性神经元 ,但是几乎未见 5 - HT免疫阳性神经元分布。(2 )在中缝核簇的大多数亚核内均可观察到大量的 NOS神经元和 5 - HT免疫阳性神经元。在中缝背核的内侧部、中缝背核的尾侧部、中缝正中核、尾侧线形核、中缝大核和中缝隐核内双标神经元分别占所在部位中 5 - HT免疫阳性神经元的 44 .6 %、5 3.4%、 44 .4%、 2 6 .2 %、 2 6 .7%和 2 1 .8%。然而在中缝苍白核内仅偶见少数双标神经元。研究结果表明 ,在 PAG和中缝核簇的一些神经元内 5 - HT可以与 NOS共存 ,提示这两种神经活性物质在功能上可能存在着某种相关性 ,有关这些双标神经元的功能意义尚需进一步研究。  相似文献   

19.
In order to study putative hypothalamic mechanisms of sleep-waking cycle regulation we injected a neural cell body toxin--ibotenic acid (IBO), 40 to 200 micrograms--into the ventrolateral part of the posterior hypothalamus (HVL). This injection induced a dramatic biphasic and transient hypersomnia immediately after the disappearance of the anesthesia (14 to 24 hours after the injection). The duration of hypersomnia was dose dependent. Its first period was characterized by an increase in paradoxical sleep (PS) (300%). Then, during the second phase, PS disappeared and there was a subsequent increase of slow sleep (SWS) (60%). Finally, on the third day, all cats recovered control level of PS and SWS while, 3 weeks later, the histological analysis revealed the great loss of cell bodies in the HVL in all cats.  相似文献   

20.
We have studied the effects of local injections of histaminergic and antihistaminic drugs on the sleep-waking cycle in the cat. Microinjections of alpha-fluoromethylhistidine (alpha-FMH), a specific inhibitor of histidine decarboxylase, in the ventrolateral posterior hypothalamus, where histamine-immunoreactive neurons have been recently identified, resulted in a significant decrease in wakefulness (W) and increase in deep slow wave sleep (SWS). On the other hand, microinjections of SKF-91488 (Homodimaprit), a specific inhibitor of histamine-N-methyltransferase, increased W and decreased SWS and paradoxical sleep (PS). Microinjections of histamine also produced an increase of W, while this effect was abolished by pretreatment with mepyramine, an H1-histamine receptor antagonist.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号