鞘内应用Ifenprodil对丘脑束旁核兴奋神经元放电的影响

在脊髓部位阻断NMDA受体对多种疼痛有镇痛效果。氯胺酮被认为是NMDA受体非特异拮抗剂。Ifenprodil特异性作用于NMDA受体NR-2B亚单位。本文通过电生理方法比较Ifenprodil和氯胺酮鞘内用药对高位中枢神经元放电的影响，探讨Ifenprodil的镇痛机制。     

纳络酮对褪黑素抑制猫丘脑后核群诱发放电的影响

目的研究阿片受体阻断剂纳络酮对褪黑素 (melatonin ,MT)中枢镇痛作用的影响 ,进一步探索MT的作用机制。方法采用猫脑立体定位技术和玻璃微电极细胞外记录法 ,以刺激内脏大神经(GSN)诱发猫丘脑后核群 (PO)单位放电为内脏痛指标 ,侧脑室给药 ,观察药效。结果侧脑室注射(icv) 4 3 0× 1 0 -3 mol·L-1MT 1 0 μg·kg-1可明显抑制刺激GSN在PO诱发的单位放电 ,2 75×1 0 -3 mol·L-1纳络酮 (5 0 μg,icv)可部分拮抗MT对PO诱发放电的抑制作用。结论MT有中枢镇痛作用 ,MT的镇痛作用与增加内源性阿片系统的活动有关     

吗啡对急性心肌缺血期大鼠丘脑束旁核神经元5-HTA受体mRNA表达的影响

目的：观察吗啡对急性心肌缺血期大鼠丘脑束旁核神经元5-HT1A受体mRNA表达的影响,探讨吗啡对急性心肌缺血伤害性刺激的作用及其机制.方法：将体重260g～280 g的健康成年雄性SD大鼠18只,随机分为三组：对照组,即非冠状动脉扎闭组（C组）,开胸后冠状动脉左前降支下穿线,不结扎;扎闭冠脉组（CAO组）,扎闭冠脉6 h;吗啡＋CAO组（MCAO组）,CAO前15 min静脉注射吗啡1.25 mg/kg,然后CAO 6 h.CAO 6 h处死动物,取含有大鼠丘脑束旁核的脑片行原位杂交.5-HT1A受体mRNA杂交结果检测采用IDA-2000数码显微图像分析系统进行半定量分析.结果：与C组比较,CAO组大鼠丘脑束旁核5-HT1A受体mRNA的表达增强（P＜0.05）,与CAO组比较,MCAO组5-HT1A受体mRNA表达降低（P＜0.05）.结论：急性心肌缺血可诱发大鼠丘脑束旁核5-HT1A受体mRNA表达增强,5-HT1A受体参与急性心肌缺血伤害性刺激在丘脑束旁核的调制,吗啡可抑制急性心肌缺血诱发的大鼠丘脑束旁核5-HT1A受体mRNA的表达增强.     

高效液相色谱法结合主成分分析法分析云芝胞内糖肽中核苷和核碱的组成

目的:本实验利用超声提取-高效液相色谱测定技术,建立了云芝胞内糖肽原料和制剂中核苷和核碱组成的检测方法.方法:样品以水为溶剂超声提取,以月旭AQ-C18柱(4.6 mm×250 mm,5μm)为填充柱,流动相为水、甲醇梯度洗脱,检测波长为260nm,流速为1.0mL·min-1,进样体积为20μL.结果:云芝胞内糖肽由...     

吗啡对急性心肌缺血期大鼠丘脑束旁核神经元5-HT_(1A)受体mRNA表达的影响

目的:观察吗啡对急性心肌缺血期大鼠丘脑束旁核神经元5-HT1A受体mRNA表达的影响,探讨吗啡对急性心肌缺血伤害性刺激的作用及其机制。方法:将体重260g~280g的健康成年雄性SD大鼠18只,随机分为三组:对照组,即非冠状动脉扎闭组(C组),开胸后冠状动脉左前降支下穿线,不结扎;扎闭冠脉组(CAO组),扎闭冠脉6h;吗啡+CAO组(MCAO组),CAO前15min静脉注射吗啡1.25mg/kg,然后CAO6h。CAO6h处死动物,取含有大鼠丘脑束旁核的脑片行原位杂交。5-HT1A受体mRNA杂交结果检测采用IDA-2000数码显微图像分析系统进行半定量分析。结果:与C组比较,CAO组大鼠丘脑束旁核5-HT1A受体mRNA的表达增强(P<0.05),与CAO组比较,MCAO组5-HT1A受体mRNA表达降低(P<0.05)。结论:急性心肌缺血可诱发大鼠丘脑束旁核5-HT1A受体mRNA表达增强,5-HT1A受体参与急性心肌缺血伤害性刺激在丘脑束旁核的调制,吗啡可抑制急性心肌缺血诱发的大鼠丘脑束旁核5-HT1A受体mRNA的表达增强。     

云芝孢内糖肽胶囊对慢性乙型肝炎临床控制后复发的影响

目的观察云芝孢内糖肽胶囊对慢性乙型肝炎临床控制后复发的影响。方法对77例慢性乙型肝炎患者,随机分为2组,治疗组加用口服云芝孢内糖肽胶囊。结果治疗组和对照组治疗前后肝功能均有显著改善。但治疗组与对照组相比,血中乙肝标志物、临床疗效及其复发史均有显著性差异。结论中医辨证施治加用云芝孢内糖肽胶囊对治疗慢性乙型肝炎临床控制后复发具有显著的疗效。     

丙泊酚对丘脑室旁核谷氨酸能神经元活性的影响

本研究利用全细胞膜片钳技术探索丙泊酚对丘脑室旁核(paraventricular thalamus, PVT)谷氨酸能神经元活性的影响及作用机制。在8周龄C57BL/6J小鼠急性脑片上,用单细胞逆转录PCR技术鉴定PVT神经元类型。记录丙泊酚给药前、后和洗脱后PVT神经元的放电频率(firing frequencies before, during, and after, FB, FD and FW)及给药前、后的膜电位(membrane potential before and during, MPB and MPD)。探索木防己苦毒素(picrotoxin, PTX)阻断γ-氨基丁酸A型(gamma-aminobutyric acid type A, GABAA)受体后对丙泊酚作用的影响,以及丙泊酚对PVT神经元上自发和微小抑制性突触后电流(spontaneous and miniature inhibitory postsynaptic currents, sIPSCs and mIPSCs)的影响。动物实验已获得复旦大学上海医学院动物实验伦理委员会批准。结果显示,在脂肪乳组和2...     

褪黑素对猫丘脑后核内脏痛放电的影响

目的观察静脉注射不同剂量褪黑素 (melatonin ,MT)对猫丘脑后核 (PO)诱发放电的影响及其存在的昼夜节律变化。方法本实验采用猫脑立体定位技术和玻璃微电极细胞外记录的方法 ,以刺激内脏大神经 (GSN)诱发PO单位放电作为内脏痛指标。结果静脉注射 1 0、1 5、2 0、2 5mg/kgMT对刺激GSN诱发的PO单簇放电均有抑制作用 ,随剂量的增大 ,抑制作用增强。对于相同的给药剂量 ( 1 5mg/kg) ,下午的镇痛时间明显较上午长 ,且存在统计学差异。 结论首次发现MT在丘脑后核水平参与抑制内脏痛 ,此抑制作用存在剂量依赖关系 ,并具有昼夜节律变化。     

染料木黄酮对大鼠下丘脑脑片室旁核神经元放电的影响(英文)

目的研究染料木黄酮(GST)在心血管中枢神经系统的作用。方法应用细胞外记录单位放电技术,在下丘脑脑片上观察GST对静息状态下的室旁核神经元放电的影响。结果①26个脑片分别灌流GST 10,50,100μmol·L~(-1)2 min,有25个脑片放电频率明显降低,且呈浓度依赖性;②用0.2 mmol·L~(-1) L-谷氨酸灌流脑片,7/7个脑片放电频率明显增加,表现为癫痫样放电,在此基础上加灌GST 50μmol·L~(-1)2 min,其癫痫样放电被抑制;③用G蛋白激活的内向整流型钾通道阻断剂四乙胺1 mmol·L~(-1)灌流脑片,约10 min后加入GST 50μmol·L~(-1),8/8个脑片的放电抑制效应被完全阻断;④用一氧化氮合酶抑制剂左旋硝基精氨酸甲酯50μmol·L~(-1)灌流脑片,7/7个脑片的放电频率增加,在此基础上加灌GST 50μmol·L~(-1)2 min,放电被抑制。结论GST可抑制下丘脑室旁核神经元自发放电,并抑制L-谷氨酸诱发的神经元癫痫样放电。这种抑制作用可能与激活G蛋白激活的内向整流型钾通道,促进K~+外流,从而引起细胞膜超极化有关;而与NO释放无关。GST可能通过降低心血管中枢的活动性而产生一定的心血管系统保护作用。     

Effects of Lesions in the Parafascicular Nucleus on Catecholamine Synthesis and Number of Muscarinic Receptor Binding Sites in the Striatum of the Rat

Abstract: Unilateral radio-frequency lesions of the parafascicular nucleus were performed in rats. Seven days, but not 24 hrs, postoperatively the following effects were observed in the ipsilateral striatum: (A) an increase in dopamine synthesis as estimated by the accumulation of DOPA following inhibition of cerebral aromatic L-amino acid decarboxylase; (B) an increase in dopamine levels and (C) a decrease in the number of muscarinic receptors binding sites using [³H] QNB as receptor ligand.     

Inhibitory effect of crotoxin on the pain-evoked discharge of neurons in thalamic parafascicular nucleus in rats.

Crotoxin (Cro), the principal neurotoxic component of Crotalus durissus terrificus, has been previously reported to have a behavioral analgesic effect in rats and mice. The present study investigated electrophysiologically the effect of Cro on pain-evoked unit discharge of neurons in thalamic parafascicular nucleus (Pf) and underlying mechanisms of its effect. The electrical discharge of Pf neurons was recorded with the microelectrode technique in rats. Intracerebroventricular (i.c.v.) injection of Cro at 0.25, 0.45 and 0.65 microg/kg resulted in a dose-dependent inhibitory effect on the pain-evoked discharge of Pf neurons. The discharge frequency and the discharge duration significantly (P<0.05) decreased after Cro administration. This inhibitory effect was significantly (P<0.05) attenuated after pretreatment with para-chlorophenylalanine (pCPA), or electrolytic lesion of dorsal raphe (DR) nucleus. In contrast, i.c.v. injection of atropine (muscarinic receptor antagonist, 5 microg) or naloxone (opioid receptor antagonist, 4 microg) had no effect on Cro-induced inhibition of discharge of Pf neurons. The results suggested that Cro has an analgesic effect, which is mediated, at least partially, by the central serotonergic system.     

Effects of transient inactivation of the subthalamic nucleus by local muscimol and APV infusions on performance on the five-choice serial reaction time task in rats

Within the basal ganglia circuitry, recent conceptions of the subthalamic nucleus are that it fulfils integrative functions. We have previously shown that bilateral excitotoxic lesions of the subthalamic nucleus induce behavioural deficits in a five-choice serial reaction time task in the rat, consistent with attentional impairments and suggesting important roles of this basal ganglia structure in mechanisms of behavioural control. In the present study, we tested the effects of (i) blocking its excitatory inputs (originating mainly in the cerebral cortex and the parafascicular nucleus of the thalamus) via the NMDA receptors and (ii) stimulating its GABA receptors to mimick the influence of its inhibitory inputs (mainly from the globus pallidus). Bilateral microinfusions of APV (NMDA receptor antagonist) or muscimol (GABA-A receptor agonist) into the subthalamic nucleus were administered to rats trained in the same five-choice serial reaction time task. Both APV (0.125–0.5 μg) and muscimol (1–3 ng) reduced choice accuracy, slowed correct responses and increased omissions and perseverative responses. Premature responses tended to increase after APV but decrease after muscimol. Increased perseverations at the food magazine occurred only after muscimol infusions. These results reproduce many of the effects of lesions of the STN and are consistent with an integrative role for this structure in pallidal and thalamo-cortical processing. Received: 19 February 1998/Final version: 12 May 1998     

氟西汀对卒中后抑郁大鼠行为学及海马神经元凋亡的影响

目的 探讨以氟西汀为代表的SSRIs对卒中后抑郁(post-stroke depression,PSD)大鼠行为学和神经元凋亡的影响。方法 用大脑中动脉线栓法(MCAO)建立大鼠局灶性脑缺血模型,再结合慢性不可预见的温和性应激(chronic unpredictable mild stress,CUMS)和孤养法建立PSD模型,加以10 mg?kg^-1氟西汀干预。比较各组大鼠体质量与糖水消耗量;旷野实验测定直立活动和水平活动得分;流式细胞仪分析神经元细胞的凋亡率。结果 应激14 d后,与PSD组大鼠比较,氟西汀干预组大鼠体质量和糖水消耗比例低(P<0.05或P<0.01),水平和垂直试验得分下降(P<0.01),海马神经元凋亡率较高(P<0.01)。结论 氟西汀对PSD有一定的治疗作用。     

Effects of polysaccharide peptides from COV-1 strain of Coriolus versicolor on glutathione and glutathione-related enzymes in the mouse.

The effects of polysaccharide peptide (PSP), an immunomodulator isolated from Coriolus versicolor COV-1, on glutathione (GSH) and GSH-related enzymes was investigated in C57 mouse. Administration of PSP (1-4 micromole/kg, i.p.) produced a transient, dose-dependent depletion (10-37%) of hepatic GSH, with no effect on serum glutamic-pyruvic transaminase (SGPT) activity. Blood GSH was depleted (6-25%) at 3 h, followed by a rebound increase above the control GSH level (20%) at 18 h. The GSSG/GSH ratio, a measure of oxidative stress, was increased 3 h after PSP treatment but returned to normal levels at 24 h. Sub-chronic treatment of PSP (1-4 micromole/kg/day, i.p.) for seven days did not produce any significant changes in hepatic GSH levels and the GSSG/GSH ratio when measured 24 h after the final dose of PSP. PSP had little effect on glutathione transferase (GST), glutathione reductase (GSSG reductase) and glutathione peroxidase (GPX) activities in the liver. However, a dose-dependent increase in blood GPX activity (30-48%) was observed at 3h, which coincided with the increase in the GSSG/GSH ratio. The increase in blood GPX activity may be a responsive measure to deal with the transient oxidative stress induced by PSP treatment. The results showed that PSP only caused a transient perturbation on hepatic glutathione without affecting the GSH-related enzymes such as GST, GSSG reductase and GPX. The observed changes in blood GSH simply reflected the intra-organ translocation of glutathione, as the glutathione-related enzymes were not significantly affected by PSP treatment.