Dopamine receptors on human T- and B-lymphocytes

The presence of functional dopamine receptors on differentiated cells of the mammalian immune system is still under discussion. This study has utilized (-)-[³H]sulpride as a ligand to detect the presence of recognition sites of the dopamine D₂ receptor family on human T- and B-lymphocytes. The (-)-[³H]sulpiride binding was of high affinity (K_d 0.9 nM ± 0.2 nM, specific, saturable (B_max 10.2 ± 1.4 fmol/10⁶ cells) and reversible. The pharmacological characterization of the recognition site suggests, similarities mainly with the D₂ and D₄ rather than D₃ subtype of dopamine receptor. Furthermore, dopamine treatment was able to reduce the intracellular cAMP levels of lymphocytes stimulated with forskolin, thus suggesting a potential functional significance of this dopamine receptor in mediating neural-immune interactions.     

Presynaptic regulation of the electrically evoked release of endogenous dopamine from the isolated neurointermediate lobe or isolated neural lobe of the rat pituitary gland in vitro

Summary Isolated neurointermediate lobes (NILs) or isolated neural lobes (NLs) of the rat pituitary gland were incubated in Krebs-HEPES solution which contained pargyline and the dopamine uptake inhibitor GBR 12921. The release of endogenous dopamine was determined by HPLC with electrochemical detection. Electrical stimulation of the pituitary stalk induced a frequency-dependent release of dopamine.The release of dopamine from the combined NIL evoked by stimulation at 15 Hz was increased by 130% in the presence of the dopamine D2 receptor antagonist, (–)-sulpiride; the (+)-enantiomer of sulpiride had virtually no effect. When the stimulation frequency was 3 Hz (–)-sulpiride caused an increase in dopamine release by 230%. A similar increase was observed in the presence of domperidone, another dopamine D2 receptor antagonist.The dopamine receptor agonists, apomorphine and quinpirole, had no significant effects on the evoked release of dopamine indicating that under the present incubation conditions endogenous dopamine may have been maximally activating the autoinhibition. However, in the presence of 1 mol/l (–)-sulpiride, apomorphine as well as quinpirole reduced the evoked release of dopamine in a concentration-dependent manner.The dopamine D1 receptor selective antagonist, SCH 23390, had no effect on the evoked release of dopamine at a concentration of 1 mol/1. Only at a concentration of 10 mol/l did SCH 23390 cause a small increase in dopamine release; this effect was, however, abolished in the presence of 1 mol/1(–)-sulpiride.In the presence of 1 mol/l (–)-sulpiride neither clonidine, yohimbine, 5-methoxytryptamine nor metitepine significantly affected the release of dopamine from the NIL evoked by stimulation at 3 Hz.In the NL, the release of dopamine is inhibited by endogenous opioids. For this reason, naloxone 1 or 10 mol/1 was present in the experiments on isolated NLs. Domperidone and (–)-sulpiride, but not (+)-sulpiride, increased the release of dopamine from the NL evoked by electrical stimulation at 15 Hz by about 90%. SCH 23390 caused a significant increase in dopamine release at 10 mol/l, but not at 1 mol/lIn conclusion, the release of endogenous dopamine from the neurons terminating in the intermediate and neural lobe of the pituitary gland is inhibited via dopamine receptors of the D2 type.Abbreviations DOPAC dihydroxyphenylacetic acid - 5-HT 5-hydroxytryptamine - HPLC high performance liquid chromatography - IL intermediate lobe - NIL neurointermediate lobe - NL neurallobe Send offprint requests to K. Racké at the above address     

舒必利与氯丙嗪合用治疗慢性精神分裂症阴性症状的对照研究

目的 探讨舒必利与氯丙嗪及舒必利,氯丙嗪治疗慢性精神分裂症阴性症状的疗效。方法 将60例以阴性症状为主要表现的慢性精神分裂症病人随机分为舒必利合并氯丙嗪组(研究组)及舒必利组,氯丙嗪3个组。用临床疗效评定标准和BPRS量表评定疗效。结果 研究组的显效率(显进 痊愈)明显比氯丙嗪组及舒必利组高,x~2检验P<0.05提示舒必利合并氯丙嗪治疗比单一用药疗效显著。舒必利组氯丙嗪组显效率比较无显著性差异(P<0.05)。结论 舒必利合并氯丙嗪治疗慢性精神分裂症阴性症状的疗效比单一用药更好,副作用更少。     

Ventromedial hypothalamus vs. lateral hypothalamic D2 satiety receptors in the body weight increase induced by systemic sulpiride

Two experiments were conducted in order to see if dopamine satiety receptors in the lateral hypothalamus or satiety mechanisms in the ventromedial hypothalamus were involved in the hyperphagia and body weight increase induced by systemic sulpiride. In the first experiment, it was shown that systemic sulpiride (20 mg/kg) does not block the anorexia caused by intraperifornical injections of amphetamine. In the second experiment, sulpiride (20 mg/kg during 18 days) did not produce an additional increase in body weight in previously VMH-lesioned female rats. This last fact cannot be explained by a ceiling effect since insulin (5 U/day during 7 days) increased body weight in the same VMH rats in which sulpiride was not effective. These results do not support the hypothesis that systemic sulpiride reaches the perifornical dopamine D2 receptors to disinhibit feeding, but suggest instead an involvement of the ventromedial hypothalamus. This last suggestion is more in agreement with the hypothesis that sulpiride alters feeding and body weight gain through the induction of a functional gonadectomy.     

抗精神病药所致体重增加的研究

目的比较典型(氯丙嗪与舒必利)与非典型抗精神病药(维思通与氯氮平)对体重的影响.方法对单服维思通、舒必利、氯氮平、氯丙嗪其中一种的精神分裂症患者,于用药前后测定体重的变化.结果服药8周后四种药物引起体重增加如下维思通组2.40kg,舒必利组2.73 kg,氯氮平组3.71 kg,氯丙嗪组4.98 kg,其中维思通组与氯丙嗪组比较差异有极显著性(P＜0.01);舒必利组与氯丙嗪组比较差异有显著性(P＜0.05).各组男女体重变化差异无显著性,但男性平均体重的增加较女性高.结论典型与非典型抗精神病药均引起体重增加,其中对体重影响从小到大为维思通＜舒必利＜氯氮平＜氯丙嗪.对体重影响的不同也导致同患病率的不同.上述各药对男女体重影响无明显不同.     

Influence of lisuride on morphine withdrawal signs in the rat: A dopamine-mimetic effect

The influence of lisuride on naloxone-induced withdrawal signs (wet shakes, escape attempts) was studied in morphine-dependent rats. Lisuride, injected IP at doses of 12.5 and 25 g/kg, inhibited wet shakes while not significantly altering escape attempts induced by naloxone (4 mg/kg IP). At higher doses (50 and 100 g/kg IP), lisuride's inhibitory effect on wet shakes persisted while escape attempts were actually potentiated with respect to control withdrawal rats. Increases in aggressive behavior were seen at all doses, and were dose-related. Haloperidol (0.3 mg/kg IP), administered 40 min before lisuride, did not modify the antagonistic effect on wet shakes, unlike sulpiride (40 mg/kg IP 30 min before lisuride), but at the same time blocked the increase in escape attempts and aggressiveness induced by lisuride. We suggest that lisuride modulates withdrawal signs by stimulation of dopamine receptors in the CNS. The effect of the dopamine mimetic N-n-propylnorapomorphine (NPA) on the same variables is reported as well as the influence of haloperidol on NPA, and a comparison between the effects of the two drugs is made.     

氨磺必利和舒必利治疗女性精神分裂症的临床效果比较

目的总结分析氨磺必利和舒必利治疗女性精神分裂症的临床效果。方法选择2013年1月～2013年12月本院收治的80例女性精神分裂症患者为研究对象,随机分为观察组和对照组,各40例,观察组给予氨磺必利治疗,对照组给予舒必利治疗,治疗2个月后,比较两组的治疗效果和不良反应。结果观察组的有效率87.50%,对照组为85.00%,两组比较差异无统计学意义（P〈0.05）;两组治疗后的PANSS评分均明显低于治疗前（P〈0.05）,但两组治疗后的PANSS评分比较差异无统计学意义（P〈0.05）;观察组的不良反应发生率为10.00%,明显低于对照组的37.50%（P〈0.05）。结论氨磺必利与舒必利对女性精神分裂症的治疗效果相当,但舒必利的不良反应发生率较高,临床要慎重选择用药。     

阿立哌唑与舒必利治疗精神分裂症的疗效及生活质量对照研究

目的探讨阿立哌唑与舒必利治疗精神分裂症的疗效及对其生活质量的影响。方法将96例精神分裂症患者随机分为阿立哌唑组和舒必利组,治疗8周,采用阳性和阴性症状量表(PAN SS)评定疗效,生活质量综合评定问卷(GDOL I)评定生活质量,副反应量表(TESS)评定不良反应。结果两组PAN SS分值治疗前后差异均有显著性(P<0.01);但两组之间比较,差异无显著性(χ2=0.3226;P>0.05)。阿立哌唑组生活质量除生活条件维度外,在躯体健康、心理健康、社会功能维度均高于舒必利组,且有显著性差异(t=2.963,3.041,2.984;P<0.01)。结论阿立哌唑与舒必利抗精神分裂症的疗效相当,但阿立哌唑对精神分裂症患者的生活质量改善明显,副反应少。     

舒必利治疗内源性抑郁

双盲对照对39例内源性抑郁进行4周观察,目的在于研究低剂量舒必剂对内源性抑郁的疗效。用汉密顿抑郁量表(HAMD)和副反应(TESS)量表评定。结果发现舒必利组与阿米替林组相比HAMD因子分减分量在第2周、第4周末无差异;TESS量表植物神经系副反应较少。本文认为低剂量舒必利与阿米替林近期抗抑郁作用相同。     

阿立哌唑与舒必利治疗以阴性症状为主的精神分裂症对照观察

目的:探讨阿立哌唑与舒必利治疗以阴性症状为主的精神分裂症患者的疗效和不良反应.方法:对60例以阴性症状为主精神分裂症患者.随机分为阿立哌唑组和舒必利组进行治疗,疗程8周.于治疗前及治疗后2、4、8周末用阴性症状量表(SANS)、简明精神病评定量表(BPRS)评定临床疗效.用不良反应量表(TESS)评定药物不良反应.结果:阿立哌唑组与舒必利组在治疗前后SANS、BPRS总分及减分率比较差异无显著性(P>0.05),各组治疗后SANS、BPRS总分与治疗前比较差异有显著性(P<0.01).阿立哌唑在必趣社交缺乏因子的疗效优于舒必利(P<0.05).结论:阿立哌唑对以阴性症状为主的精神分裂症有肯定的疗效,在某些方面优于舒必利,安全性较高.