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81.
The effects of serotonin were studied on locust-killing behavior of mice from low (DD) and high (CBA) predatory aggressive strains. 5-HTP injected intraperitoneally (50 and 100 mg/kg) or 5-HT administered into the lateral ventricle (10 μg) significantly reduced locust-killing behavior in highly aggressive CBA mice. Imipramine (20, 30, and 40 mg/kg) elicited a dose-dependent inhibitory effect on predatory behavior. Fluoxetine (10 and 20 mg/kg) alone had a slight influence on locust-killing behavior but potentiated the action of the subthreshold dose of 5-HTP (25 mg/kg). Pretreatment with the blocker of 5-HT2 type receptors methysergide (2 mg/kg) abolished the inhibitory effect of 5-HTP. These finding indicate that serotonin of the brain exerts an inhibitory effect on predatory behavior in mice. In contrast, neither lesion of the dorsal raphe nucleus (although significantly depleting the brain serotonin) nor treatment with methysergide (2 mg/kg) induced locust-killing behavior in weakly aggressive DD mice. Low predatory aggressiveness in DD mice is suggested to be related to the low tonus of the mechanisms activating killing behavior rather than to excessive serotonergic inhibitory influences.  相似文献   
82.
This study aimed to evaluate a peripheral serotonergic marker, 3H-imipramine (3H-IMI) binding to platelet membranes, in a group of severely aggressive subjects (A), institutionalized since childhood for mental retardation, as compared with suicide attempters (S) and healthy controls (H). The maximum binding capacity of 3H-IMI to platelet membranes was statistically lower in (A) and (S) than in (H). In addition, a statistically significant difference was observed between the Bmax values of aggressive subjects and those of suicide attempters. No changes in the dissociation constant (Kd) of IMI binding were observed. These data provide further supporting evidence for the hypothesis of an abnormality of the 5HT system in aggressive behaviour and suggest that such an abnormality, as reflected by platelet markers, is more severe in suicide attempters. © 1993 Wiley-Liss, Inc.  相似文献   
83.
恐惧消退能力的受损是创伤后应激障碍(posttraumatic stress disorder, PTSD)的标志之一。以往的研究表明, 相较于延迟消退, 恐惧获得后短时间内进行的消退训练不能形成长时程的消退记忆, 这一现象被称为即刻消退缺损。然而, 目前并不清楚这种缺损是一次性的, 还是会继续影响其后的重消退。实验1中, 大鼠在恐惧习得后1小时(即刻消退)或24小时(延迟消退)开始进行消退训练, 24小时后进行重消退, 再24小时后进行消退记忆的测试。结果显示, 与延迟消退相比, 即刻消退效果缺损, 并引起第二天的重消退也出现效果缺损。实验2中, 恐惧获得后立即给予大鼠盐水或β-肾上腺素受体阻断剂普萘洛尔(10 mg/kg, i.p.), 然后测试即刻消退和重消退的效果。结果显示, 普萘洛尔虽没有阻止即刻消退的缺损, 但避免了重消退出现缺损。总之, 严重创伤后的即刻消退不但无法有效抑制恐惧反应, 还可能造成二次创伤, 会损害恐惧消退能力, 而普萘洛尔可修复即刻消退引起的重消退缺损。这些结果将有助于我们加深对PTSD病理机制和早期干预后果的认识。  相似文献   
84.
精神分裂症是一种常见的病因不明的精神疾病。大量文献表明精神分裂症患者所表现出来的认知紊乱和思维异常等症状与感觉门控功能的缺失有密切的关系, 感觉门控是指在充满刺激的环境中, 从外界的感觉信息中过滤无关的感觉信息然后执行与注意力相关的认知过程, 以对显著的刺激做出反应。研究感觉门控的经典范式是震惊反射的前脉冲抑制。研究发现多巴胺D2受体可以参与调控前脉冲抑制的过程, 但是多巴胺D2受体参与调控前脉冲抑制的机制仍不清楚。探讨多巴胺D2受体参与调控感觉门控即前脉冲抑制的关键脑区、神经环路及分子机制, 有利于促进对精神分裂症感觉门控功能的深入研究。  相似文献   
85.
早期环境因素持续影响脑与行为的发展,增加个体成年后应激相关精神疾病患病的易感性.应激反应的中枢启动因子促肾上腺皮质激素释放因子(corticotropin-releasing factor,CRF)通过两种受体CRF1和CRF2调节中缝背核(dorsal raphe nucleus,DRN)-五-羟色胺(serotonin,5-HT)系统,后者已被证实在应激相关情绪疾患发病和治疗过程中发挥重要作用.已知CRF受体以相互影响相互拮抗的方式动态调节DRN-5-HT系统,提示这两种受体相对作用的调节对于协调复杂环境中DRN-5-HT系统的应激反应过程起着关键性作用.早期环境因素和遗传因素交互作用导致CRF受体的分布和反应性持续改变并造成DRN-5-HT系统反应异常,可能是导致应激反应和精神疾病易感性个体差异的重要神经基础.  相似文献   
86.
抑郁症的发病存在多种假说,其中较为公认的有细胞因子假说,下丘脑-垂体-肾上腺皮质(hypothalamus-pituitary-adrenocortical,HPA)轴假说,单胺能假说,神经可塑性假说等,不同假说可能从不同角度探讨抑郁症的病理机制,但各种假说都与吲哚胺2,3-双加氧酶(indoleamine 2,3-dioxygenase,IDO)的调节有关。IDO是一种色氨酸降解酶,其活性能够被前炎性细胞因子所增强。IDO活性的增强使色氨酸更多地代谢为犬尿氨酸(kynurenine,KYN),从而可能导致生成5-羟色胺(serotonin,5-HT)的原料不足,5-HT生成减少。而且,色氨酸-犬尿氨酸代谢通路的下游产物犬尿喹啉酸(kynurenicacid,KYNA),喹啉酸(quinolinic acid,QUIN)及3-羟基犬尿氨酸(3-hydroxykynurenine,3HKYN)等影响神经元的再生与退化。另外,应激激素也可以通过色氨酸2,3-双加氧酶(tryptophan 2,3-dioxygenaes,TDO)或免疫系统影响IDO的功能。IDO是抑郁症多种假说病理机制中的共同调节因子,可能在抑郁病的发病中具有重要作用。  相似文献   
87.
聊城市汉族正常人血清骨钙素参考值的研究   总被引:1,自引:0,他引:1  
建立聊城市汉族正常人血清骨钙素水平的参考值。利用化学发光免疫分析法对聊城市162例汉族体检健康者血清骨钙素(BGP)水平进行检测,检测范围0.2ng/ml-100ng/ml。结果聊城市汉族正常人血清骨钙素水平的参考值为5.21±0.73ng/ml。首次报道了聊城市汉族正常人血清骨钙素参考值,为骨病骨代谢研究提供一项新的...  相似文献   
88.
89.
Manning, Bundred, Newton, and Flanagan reported a significant correlation of .29 in a sample of 50 British males between the length of a repeated sequence on the androgen receptor gene and 2D:4D finger-length ratio on the right hand. We report a 2nd failure to replicate this result. Ours was a sample of 182 Australian male twins studied for other purposes, for whom both measures were available. The result was a nonsignificant correlation of −.055. A similar result was obtained for female twins, and for comparisons within sibling pairs. Correlations are also reported for left hands and right-left differences--the last showed a weak tendency toward replication.  相似文献   
90.
A recent phylogenetic analysis of two learning-related neuromodulatory traits in mechanosensory neurons of species related to the marine molluskAplysia californicaidentified one species,Dolabrifera dolabrifera,which lacked both neuromodulatory traits. Since these traits are thought to contribute importantly to certain forms of learning and memory in the defensive withdrawal reflexes ofAplysia,in the present study, I tested the prediction that facilitatory nonassociative learning would be reduced or absent inDolabrifera.I tested the tail-mantle withdrawal reflex inDolabriferaand size-matchedAplysiafor three forms of nonassociative learning and memory: dishabituation and short- and long-term sensitization. I found that the same protocols that produced significant dishabituation, short-term sensitization, and long-term sensitization inAplysiafailed in all three cases to produce significant learning inDolabrifera.Thus, the prediction from the prior mechanistic analysis is confirmed: Dishabituation and short- and long-term sensitization are significantly reduced and perhaps abolished inDolabrifera.Although not conclusive, this phylogenetic correlation between the absence of behavioral changes and the absence of neural mechanisms thought to underlie the behavioral changes gives support to the contemporary neuromodulatory model of dishabituation and sensitization inAplysia.Furthermore, these results raise the possibility that evolutionary alteration of two specific neuromodulatory mechanisms may have directly contributed to evolutionary change in behavioral plasticity.  相似文献   
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