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1.
Acute selective serotonin reuptake inhibitors increase conditioned fear expression: blockade with a 5-HT(2C) receptor antagonist. 总被引:3,自引:0,他引:3
Nesha S Burghardt David E A Bush Bruce S McEwen Joseph E LeDoux 《Neuropsychopharmacology》2007,62(10):1111-1118
BACKGROUND: Selective serotonin reuptake inhibitors (SSRIs) effectively treat various anxiety disorders, although symptoms of anxiety are often exacerbated during early stages of treatment. We previously reported that acute treatment with the SSRI citalopram enhances the acquisition of auditory fear conditioning, which is consistent with the initial anxiogenic effects reported clinically. Here, we extend our findings by assessing the effects of acute SSRI treatment on the expression of previously acquired conditioned fear. METHODS: Rats underwent fear conditioning drug-free. Tone-evoked fear responses were tested after drug treatment the following day. This protocol more closely resembles the clinical setting than pre-conditioning treatment, because it evaluates effects of treatment on a pre-existing fear rather than on the formation of a new fear memory. RESULTS: A single pre-testing injection of the SSRIs citalopram or fluoxetine significantly increased fear expression. There was no effect of the antidepressant tianeptine or the norepinephrine reuptake inhibitor tomoxetine, indicating that this effect is specific to SSRIs. The SSRI-induced enhancement in fear expression was not blocked by tropisetron, a 5-HT(3) receptor antagonist, but was blocked by SB 242084, a specific 5-HT(2C) receptor antagonist. CONCLUSIONS: Enhanced activation of 5-HT(2C) receptors might be a mechanism for the anxiogenic effects of SSRIs observed initially during treatment. 相似文献
2.
为研究5-羟色胺(5-HT)能神经递质在癫痫形成过程中的变化及西酞普兰(CTP)对其的影响,本研究用CTP(1mg/kg.d灌胃)预干预1周后,对戊四氮(PTZ,30mg/kg.d,腹腔注射)点燃癫痫过程中的行为学及在不同时间点对大鼠海马进行微透析取样,经高效液相电化学检测技术在活体观察了30只自由活动大鼠5-HT及其代谢产物5-羟吲哚乙酸(5-HIAA)水平和5-HT转化率(5-HIAA/5-HT)的动态变化。结果显示:PTZ注射后在CTP组发作潜伏期延长,发作程度轻和点燃时间延长,发作死亡率降低。点燃早期,CTP组大鼠的海马5-HT水平升高,5-HT转化率降低,与对照组和PTZ组比较,有显著性差异(P<0.05);点燃晚期CTP组和PTZ组与对照组比较5-HT水平和5-HT转化率均显著降低(P<0.05)。本研究结果提示PTZ点燃过程中,早期CTP升高脑内5-HT水平,可能直接抑制了引起爆发放电的动作电位,而抑制发作;晚期脑内5-HT神经元丢失和受体减少,功能减退,而导致CTP的作用减退。 相似文献
3.
Ro 11-2465 (cianopramine, cyan-imipramine) and citalopram (CIT), putative antidepressant drugs, are very potent and selective 5-hydroxytryptamine (5-HT) uptake inhibitors in vitro. This study investigated the effects of these drugs and their desmethyl metabolites, Ro 12-5419 (desmethylcianopramine, cyan-desipramine) and desmethylcitalopram (DCIT), respectively, on the uptake of 5-HT and noradrenaline (NA) in vivo [protection against H 77/77 (4, alpha-dimethyl-metatyramine)-induced displacement of 5-HT and NA] and on related pharmacological activities. All the investigated drugs antagonized H 77/77-induced displacement of 5-HT in the rat brain, though the effects of the metabolites were considerably weaker than those of the parent compounds. The H 77/77-induced displacement of brain NA in rats and mice was antagonized only by Ro 12-5419 and Ro 11-2465. All the drugs potentiated the pressor response to 5-HT in pithed rats; however, Ro 12-5419 and particularly Ro 11-2465 could also block the response when used in higher doses (0.1 mg/kg). Only Ro 12-5419 and Ro 11-2465 were able to potentiate the pressor response to NA. Ro 12-5419 also potentiated thyrotropin releasing hormone (TRH) hyperthermia and antagonized reserpine hypothermia in mice; Ro 11-2465 potentiated the TRH hyperthermia only. CIT and DCIT were inactive in both these tests. Of all the four drugs only CIT and Ro 12-5419 considerably stimulated the hind limb flexor reflex in spinal rats. However, whereas the stimulatory effect of CIT was inhibited by the 5-HT antagonists metergoline and cyproheptadine, that of Ro 12-5419 was counteracted by the NA antagonist phenoxybenzamine only. Ro 11-2465, when used in low doses (ca. 1 mg/kg), slightly potentiated the flexor reflex, whereas in higher doses (4–16 mg/kg) it had no effect itself but antagonized the stimulatory action of the 5-HT agonists fenfluramine, quipazine and LSD. The results obtained indicate that Ro 11-2465 and CIT, as well as their desmethyl metabolites, are also potent 5-HT uptake inhibitors in vivo. However, only CIT and DCIT are concurrently devoid of effect on uptake of NA. In contrast, Ro 11-2465 and particularly Ro 12-5419 appear to also inhibit the uptake of NA. Moreover, Ro 11-2465 appears to block central and peripheral 5-HT receptors.The results were presented at the 14th CINP Congress, Florence, June 19–23, 1984 相似文献
4.
HPLC-MS同时测定4种新型抗抑郁药物的血药浓度 总被引:12,自引:1,他引:12
目的:建立一种快速灵敏的同时测定血浆中氟西汀、西酞普兰,帕罗西汀及文拉法辛浓度的 HPLC-MS 方法,监测这4种药物的血药浓度,为临床用药提供依据。方法:以氟伏沙明作为内标,样品碱化后固相萃取,用 MACHEREY-NAGEL C_(18)反相色谱柱(4.6 mm×250 mm,5μm,Germany)进行分离,以乙腈-缓冲盐(30 mmol 醋酸铵和0.6‰甲酸)(65:35)为流动相,柱温40℃,流速0.85 mL·min~(-1)。采用质谱电喷雾电离源(ESI)将样品离子化,选择性离子监测(SIM)准分子离子峰。结果:氟西汀、西酞普兰、帕罗西汀,文拉法辛及内标氟伏沙明在9 min 内完全分离;各物质在5~1000 ng·mL~(-1)时线性关系良好,相关系数均大于0.9964;萃取回收率均大于73.2%;方法回收率均大于95.0%;最低检测浓度:氟西汀0.5 ng·mL~(-1)、西酞普兰0.3 ng·mL~(-1)、帕罗西汀0.3 ng·mL~(-1),文拉法辛0.1 ng·mL~(-1);日内日间变异系数均小于15%。结论:本方法简便快速,灵敏准确,可用于血药浓度的临床监护、中毒分析,药物动力学以及代谢机制的研究。 相似文献
5.
人血浆中西酞普兰的HPLC-荧光法测定 总被引:2,自引:1,他引:2
建立了HPLC-荧光法测定人血浆中西酞普兰的浓度.血浆样品经液-液萃取后测定,用Zorbax SB C8色谱柱,磷酸二氢铵缓冲液(pH 3.5)-乙腈(65:35)为流动相,激发波长240 nm,发射波长302 nm.血浆中西酞普兰线性范围为1~100ng/ml,最低定量浓度为1ng/ml,日内、日间RSD均小于4.0%,方法平均回收率为93.2%. 相似文献
6.
5-氰基异苯并呋喃-1-酮的合成 总被引:1,自引:0,他引:1
邻苯二甲酰亚胺经硝化、还原制得4-氨基邻苯二甲酰亚胺,还原1个羰基后加热脱氨并环合制得5-氨基异苯并呋喃-1-酮,最后经Sandmeyer反应进行氰基取代制得5-氰基异苯并呋喃-1-酮,总收率39%. 相似文献
7.
8.
目的:评价米氮平与西酞普兰治疗双相抑郁的疗效及安全性.方法:将符合中国精神障碍分类与诊断标准第3版双相抑郁诊断标准的64例患者随机分为两组,予米氮平(32例)及西酞普兰(32例)分别合并碳酸锂治疗,疗程为12周.采用汉密尔顿抑郁量表(HAMD)、躁狂量表(BRMS)、临床疗效总评量表(CGI)评定疗效,以治疗中出现的症状量表(TESS)评定不良反应.结果:治疗12周后,两组患者HAMD、CGI评分均显著减少(P<0.05或P<0.01),BRMS、TESS评分均无明显增加.两组间比较HAMD、CGI、BRMS、TESS评分差异无显著性(P>0.05).结论:米氮平与西酞普兰治疗双相抑郁均有较好的疗效,不良反应较少,无诱发躁狂病例. 相似文献
9.
目的建立高效液相色谱法测定西酞普兰血药浓度。方法采用液-液萃取法,用正己烷-异戊醇(98:2)提取血浆中西酞普兰,选用普萘洛尔为内标。色谱柱为NucleodurCN(4.6mm×250mm,5μm),流动相:乙腈-30mmol·L-1KH2PO4缓冲液(0.1%三乙胺,pH5.0)(40:60),激发波长:236nm,发射波长:306nm,流速:1.3ml·min-1,柱温:室温。结果本法线性范围在1-75μg·L-1(r=0.9996)。平均方法回收率为(96.8±5.0)%(n=15),日内RSD≤8.6%,日间RSD≤9.6%。结论本法简单、快速、准确,可用于临床血药浓度监测及人体药动学研究。 相似文献
10.
目的以简单易得的原料合成西酞普兰的中间体5-腈基异苯并呋喃-1-酮。方法以邻苯二甲酰亚胺为原料,通过硝化、还原、开环、环合、Sandmeyer反应、取代等6步反应制得5-腈基异苯并呋喃-1-酮。结果目标化合物经熔点测定、红外光谱、核磁共振氢谱等确证其化学结构。结论原料易得,方法简单,值得推广。 相似文献