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可乐定镇痛与中枢Ca~(2+)的关系 总被引:1,自引:0,他引:1
用大鼠甩尾法和放射配基结合实验,探讨了可乐定镇痛与中枢Ca~(2+)的关系。CaCl_2(1μmol/rat,icv)和EGTA(0.2μmol/rat,icv)分别拮抗和增强可乐定(1mg/kg,sc)的镇痛。戊脉安(0.1μmol/rat,icy)对可乐定(1 mg/kg,sc)镇痛无明显影响,但可部分翻转CaCl_2对可乐定镇痛的拮抗。CaCl_2(1×10~(-3)mol)对[~3H]-可乐定结合无明显抑制。结果表明可乐定镇痛与脑室周围组织中Ca~(2+)浓度变化密切相关,Ca~(2+)至少部分需经对戊脉安敏感的钙通道进入细胞内方可拮抗可乐定镇痛。推沦:可乐定镇痛与神经元内Ca~(2+)有关。 相似文献
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本文通过小鼠光辐射热甩尾实验证明毛果芸香碱对可乐定镇痛具有增强作用,而阿托品则具有拮抗作用。阿托品对可乐定镇痛的拮抗可能不是通过竞争受体的机制,因阿托品只有达10~(-4)M/L时方可减少(~3H)-可乐定的特异性结合。给大鼠侧脑室注射密胆碱(30μg/只)明显减弱可乐定(2mg/kg,S·C)的镇痛效应。结果提示可乐定镇痛效应的充分发挥需要中枢胆碱能系统功能的完整。 相似文献
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目的 研究四肽FMRFa对大鼠单个心室肌细胞Na+/Ca2+交换的作用。方法 用膜片钳全细胞记录法测定成年大鼠心室肌细胞Na+/Ca2+交换电流(INa+/Ca2+)和其他离子通道电流。结果 FMRFa对大鼠心室肌细胞INa+/Ca2+呈浓度依赖性抑制,100μmol·L-1浓度时抑制内向和外向INa+/Ca2+密度分别达60.1%和56.5%,对内向电流及外向电流的IC50分别为20μmol·L-1和34μmol·L-1。FMRFa5μmol·L-1抑制INa+/Ca2+内向和外向电流密度分别为38.7%和34.9%,但FMRFa5μmol·L-1及20μmol·L-1对L型钙电流、钠电流、瞬时外向电流和内向整流钾电流均无显著抑制作用。结论 FMRFa对大鼠心室肌细胞是一个特异性Na+/Ca2+交换抑制剂。 相似文献
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赛庚啶对离体犬心肌肌质网Ca2+,Mg2+—ATP酶活性和45Ca2+摄取功能的影响 总被引:3,自引:0,他引:3
当赛庚啶浓度在8×10-6mol/L~2×10-4mol/L之间时,该药对正常犬心肌肌质网Ca2+,Mg2+—ATP酶活性几乎没有影响,仅在10-3mol/L时对该酶活性才有一定的抑制作用(抑制率为39.85%,P<0.01)。正常犬心肌肌质网的45Ca2+摄取过程有明显的时间依赖性,至第30 min,其45Ca2+摄取量可达312.79±22.25 nmol/mg protein.赛庚啶对心肌肌质网的~(45)Ca2+摄取有一定的抑制作用,其IC50为1.94×10-4mol/L。 相似文献
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观察了多次海马内微注射NGF对小鼠突触体内游离钙水平的影响,并在离体情况下观察NGF对EGTA和CaCl2分别造成突触体内低钙和高钙状态的调节作用。结果如下:(1)在体实验表明,一定剂量的NGF可显著降低老年小鼠海马突触体内游离钙水平(P<0.05);(2)离体实验表明,当突触体游离钙水平降低时,适当剂量的NGF具有升高游离钙水平的作用;而突触体内游离钙水平升高时,则NGF有降低游离钙水平的作用。提示NGF对游离钙水平的双向调节作用可能是NGF改善老年性记忆衰退的作用机制。 相似文献
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运用Ca2+指示剂Fura-2作为细胞内钙离子的荧光探针,利用AR—CM—MIC阳离子测定系统,检测了分离的神经细胞内游离钙及其变化,并观测了DGAVP和Org2766对蛋白质合成抑制剂茴香霉素(ANI)引起细胞内钙离子浓度([Ca2+]i)变化的影响。结果表明茴香霉素可使[Ca2+]i显著升高,且有量效关系;DGAVP本身并不引起[Ca2+]i发生显著变化,但适当剂量的DGAVP可显著对抗一定剂量范围内ANI升高[Ca2+]i的作用,提示DGAVP对抗ANI的蛋白质合成抑制效应可能是通过拮抗ANI升高[Ca2+]i这一途径实现的,另一神经肽Org2766则可能不是通过这一机制发生作用。从细胞内Ca2+的角度看,这两种肽的作用机理显然是不同的。 相似文献
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前胡香豆素对肾型高血压大鼠左室肥厚及心肌胞内钙、Na+,K+-ATP酶和Ca2+,Mg2+-ATP酶活性的影响 总被引:8,自引:1,他引:8
目的研究前胡香豆素组分对肾型高血压左室肥厚的预防和逆转作用及机制。方法用两肾一夹肾型高血压左室肥厚大鼠(RHR)模型,测定前胡香豆素组分对其血压、左室湿重、心肌细胞面积、胞内静息钙及胞膜和线粒体ATP酶活性的影响。结果前胡香豆素组分(30 mg·kg-1·d-1,ig)预防组及逆转组大鼠血压、左室湿重/体重均较肥厚组明显降低;左室心肌细胞面积、胞内静息钙均较肥厚组降低;对KCl致钙浓度升高亦明显低于肥厚组;两组均可增加心肌细胞膜及线粒体Na+,K+-ATP酶和Ca2+,Mg2+-ATP酶活性。结论前胡香豆素组分可预防及逆转RHR左室肥厚,减少心肌细胞内钙含量,增加ATP酶活性。 相似文献
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丹皮酚磺酸钠对钙反常培养乳鼠心肌细胞Ca2+内流的抑制作用 总被引:4,自引:0,他引:4
培养乳鼠心肌细胞复制钙反常模型,观察丹皮酚磺酸钠对心肌细胞45Ca摄取、膜唾液酸(SA)含量及细胞搏动频率的影响,结果提示丹皮酚磺酸钠在50~400μg/ml范围内能显著抑制正常心肌细胞快相(5 min)和慢相(120 min)45Ca摄取及其搏动频率,且能显著抑制钙反常心肌细胞的452+内流外,尚与其提高膜SA含量有关。 相似文献
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Dirk H. G. Versteeg Tamás Csikós Henk Spierenburg 《Naunyn-Schmiedeberg's archives of pharmacology》1991,343(6):595-602
Summary The periaqueductal gray is a brain region of considerable interest. It is innervated by monoamine-containing neurons as well as by a variety of peptidergic fiber systems, and it participates in the regulation of various functions. Virtually nothing is known about monoamine release in the periaqueductal gray and its receptor-mediated modulation. We therefore studied the release of radioactivity from periaqueductal gray slices preloaded with tritriated monoamines, using an in vitro superfusion method.The release of radioactivity from superfused periaqueductal gray slices after preloading of the tissue with [3H]noradrenaline increased upon electrical stimulation in a frequency-dependent manner. The stimulus-evoked release of radioactivity was Ca2+-dependent. Clonidine reduced and yohimbine enhanced the release. The inhibition curve for the effect of clonidine was shifted to the right in the presence of 10–6 M yohimbine. While phenylephrine, isoprenaline, SK&F 38393, quinpirole, carbachol, [Arg8]vasopressin, -MSH and ACTH-(1-24), at a concentration of 10–6 M, did not influence the electrically evoked release of radioactivity, [Leu5]enkephalin reduced it. The selective -opioid receptor agonists [d-Ala2,NMePhe4,Gly-ol5]enkephalin and [d-Arg2,Lys4]-dermorphin-(1–4)-amide reduced the release of radioactivity, whereas the selective opioid receptor agonist [d-Pen2,d-Pen5]enkephalin and the selective K opioid receptor agonist U-69593 had no effect. In the presence of naloxone, which by itself had no effect on the release of radioactivity, the effect of [d-Arg2,Lys4]dermorphin-(1–4)-amide was abolished. These results show that the release of noradrenaline from periaqueductal gray slices is via a Ca2+-dependent. exocytotic process, and that it is modulated through 2-adrenoceptors as well as via -opioid receptors. Though the overflow of radioactivity from slices preloaded with [3H]dopamine in the presence of desipramine was measurable, there are reasons to assume that we are dealing here with the release of tritiated catecholamines from a population of nerve endings consisting of noradrenergic and dopaminergic terminals.The release of radioactivity from periaqueductal gray slices preloaded with [3H]5-hydroxytryptamine upon elevation of the K+ concentration in the superfusion medium was much more pronounced than that induced by electrical stimulation. The K+-evoked release of radioactivity was almost completely abolished in the absence of Cat2+; showing that the release is via a Ca2+-dependent process. 5-Hydrotryptamine reduced the K+-evoked release of radioactivity in a concentration-dependent manner.Some of these data were presented at the XIth International Congress of Pharmacology, 1–6 July 1990, Amsterdam, The Netherlands (Eur J Pharmacol 183:408)
Send offprint requests to D. H. G. Versteeg at the above address 相似文献
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I. Wessler A. Klein D. Pohan J. Maclagana K. Racké 《Naunyn-Schmiedeberg's archives of pharmacology》1991,344(4):403-411
Summary Basal and stimulated outflow of radioactive acetylcholine, phosphorylcholine and choline from rat and guinea-pig isolated tracheae were measured by reverse phase HPLC followed by liquid-scintillation-spectrometry. Tracheae were stimulated either by an electrical field (transmural stimulation) or by a local stimulation of the innervating parasympathetic nerves (preganglionic stimulation). Epithelium was removed in most experiments, as the epithelium inhibits acetylcholine release.The basal tritium efflux (1,600 dpm/3min) from rat isolated tracheae incubated with [3H]choline consisted of 56% [3H]phosphorylcholine and 38% [3H]choline. Preganglionic stimulation (15 Hz, 1,200 pulses) caused a 2-fold increase in tritium outflow that was abolished by the removal of extracellular calcium or by the addition of tetrodotoxin. The stimulated outflow of tritium induced by preganglionic nerve stimulation was caused by an exclusive release of [3H]acetylcholine, whereas the efflux of [3H]phosphorylcholine and [3H]choline remained unaffected by this stimulation mode. Transmural stimulation of the rat or guinea-pig trachea, however, caused, in addition to the release of [3H]acetylcholine, the outflow of [3H]phosphorylcholine. Hexamethonium (300 mol/l) or tubocurarine (100 mol/l) inhibited (80%) the increase in tritium outflow evoked by preganglionic stimulation, but did not affect tritium outflow evoked by transmural stimulation. Oxotremorine reduced [3H]acetylcholine release evoked by both stimulation modes, but oxotremorine was less potent with transmural stimulation. Scopolamine (0.3 mol/l) enhanced (120%) the release of [3H]acetylcholine evoked by preganglionic nerve stimulation indicating the blockade of an endogenous negative muscarinic feedback mechanism. Epithelium-dependent inhibition of [3H]acetylcholine release was evident with both preganglionic and transmural stimulation.The present experiments demonstrate the release of [3H]acetylcholine evoked from the isolated trachea by stimulation of the preganglionic trunk of the parasympathetic cholinergic nerves. Qualitative and quantitative differences were observed in comparison to transmural stimulation. Preganglionic nerve stimulation allows a selective excitation of pulmonary, parasympathetic nerve fibres, mimics the physiological excitation of intramural neurones and is not followed by the liberation of phosphorylcholine from non-neuronal cells.
Send offprint requests to I. Wessler at the above address 相似文献
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Kevin M. Lawrence Jan Falkowski Robin R. Jacobson Roger W. Horton 《Psychopharmacology》1993,110(1-2):235-239
Platelet 5-HT uptake sites were measured in 40 depressed patients and 40 controls using [3H] imipramine binding, defined with desmethylimipramine (DMI) and Na+ dependence, and [3H] paroxetine binding. In control subjects the Bmax of DMI defined [3H] imipramine binding was significantly higher than both Na+ dependent [3H] imipramine (by 30%) and [3H] paroxetine binding (by 22%). The Bmax of Na+ dependent [3H] imipramine and [3H] paroxetine binding did not differ significantly. The Kd of Na+ dependent [3H] imipramine binding was significantly lower than the Kd of DMI defined [3H] imipramine binding. The binding of DMI defined and Na+ dependent [3H] imipramine and [3H] paroxetine did not differ significantly between depressed patients and controls in the total group, in those depressed patients who had never taken antidepressants or in those depressed patients who had been recently with-drawn from antidepressants. This study provides no support for the view that the number of platelet 5-HT uptake sites are reduced in depression. 相似文献
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Mario Marchi Adriano Augliera Agnese Codignola Gianluigi Lunardi Ernesto Fedele Giovanni Fontana Maurizio Raiteri 《Naunyn-Schmiedeberg's archives of pharmacology》1991,344(3):275-280
Summary Dendrosomes prepared from substantia nigra are able to take up and release [3H]dopamine in a Ca2+-dependent manner. The Vmax values of [3H]dopamine uptake in substantia nigra dendrosomes was about 5 times lower than that in caudate putamen synaptosomes. The pattern of the K+-dependency of the [3H]dopamine release in substantia nigra dendrosomes was significantly different from that found in caudate putamen synaptosomes. The release of [3H]dopamine evoked by 15 mmol/l KCl from superfused dendrosomes was increased in a concentration-dependent manner by acetylcholine. The maximal potentiation produced by acetylcholine was about 40%. The potentiation of [3H]dopamine release by 10 µmol/l acetylcholine was insensitive to mecamylamine but antagonized by atropine and by pirenzepine. The effects of acetylcholine on the release of [3H]acetylcholine from substantia nigra nerve endings was also studied. Exogenous acetylcholine added to the superfusion medium decreased in a concentration-dependent manner the release of acetylcholine. This effect was not antagonized by mecamylamine or pirenzepine but fully antagonized by atropine. The data suggest the existence, in the substantia nigra of the rat, of two distinct muscarinic receptor subtypes regulating respectively dopamine release from dopamine dendrites and acetylcholine release from cholinergic nerve terminals.Part of this work was presented at a satellite meeting of the 11th International Congress of Pharmacology: Dopamine '90 held in Como, Italy (July 1990)
Send offprint requests to M. Raiteri at the above address 相似文献
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A. Zharkovsky A. M. Tötterman J. Moisio L. Ahtee 《Naunyn-Schmiedeberg's archives of pharmacology》1993,347(5):483-486
Summary The effect of chronic administration of dihydropyridine calcium channel antagonist nimodipine (1 mg/kg/day) given concurrently with morphine on the signs of morphine withdrawal and on the [3H]nitren-dipine binding in the rat brain has been investigated. Chronic morphine administration in increasing daily doses from 20 mg/kg to 70 mg/kg for 24 days and consequent withdrawal for 24 h induced loss of body weight, wet dog shakes, episodes of writhing and yawning behaviour. The density of [3H]nitrendipine binding was elevated in the cortex and limbic structures but not in the striatum after chronic morphine treatment. Chronic concurrent administration of nimodipine prevented the loss of body weight and reduced the scores of wet dog shakes and writhing, but did not affect yawning behaviour at 24h after morphine withdrawal. The concurrent nimodipine treatment also prevented the rise in the density of central dihydropyridine binding sites which occurred upon chronic morphine treatment. These results suggest that chronic nimodipine treatment attenuates the development of the withdrawal signs which occur upon the termination of chronic morphine treatment by preventing the up-regulation of the central dihydropyridine-sensitive binding sites.
Correspondence to: L. Ahtee at the above address 相似文献