The post-ictal immobility syndrome is followed by a significant increase in the nociceptive thresholds in animals and men. In this interesting post-ictal behavioral response, endogenous opioid peptides-mediated mechanisms, as well as cholinergic-mediated antinociceptive processes, have been suggested. However, considering that many serotonergic descending pathways have been implicated in antinociceptive reactions, the aim of the present work is to investigate the involvement of 5-HT(2)-serotonergic receptor subfamily in the post-ictal antinociception. The analgesia was measured by the tail-flick test in seven or eight Wistar rats per group. Convulsions were followed by statistically significant increase in the tail-flick latencies (TFL), at least for 120 min of the post-ictal period. Male Wistar rats were submitted to stereotaxic surgery for introduction of a guide-cannula in the rhombencephalon, aiming either the nucleus raphe magnus (NRM) or the gigantocellularis complex. In independent groups of animals, these nuclei were neurochemically lesioned with a unilateral microinjection of ibotenic acid (1.0 microg/0.2 microL). The neuronal damage of either the NRM or nucleus reticularis gigantocellularis/paragigantocellularis complex decreased the post-ictal analgesia. Also, in other independent groups, central administration of ritanserin (5.0 microg/0.2 microL) or physiological saline into each of the reticular formation nuclei studied caused a statistically significant decrease in the TFL of seizing animals, as compared to controls, in all post-ictal periods studied. These results indicate that serotonin input-connected neurons of the pontine and medullarly reticular nuclei may be involved in the post-ictal analgesia.

译文

发作期后不动综合症之后,动物和男性的伤害性阈值显着增加。在这种有趣的发作期后行为反应中,已经提出了内源性阿片肽介导的机制以及胆碱能介导的抗伤害感受过程。然而,考虑到许多血清素能下降途径与抗伤害感受反应有关,因此本工作的目的是研究5-HT(2)-血清素能受体亚家族在发作期抗伤害感受中的参与。每组7或8只Wistar大鼠通过甩尾试验测量镇痛效果。抽搐后,至少在发作后的120分钟内,甩尾潜伏期 (TFL) 具有统计学上的显着增加。雄性Wistar大鼠接受立体定向手术,以在菱形脑中引入引导套管,以瞄准中缝大核 (NRM) 或千兆体复合体。在独立的动物组中,这些核通过单侧微量注射ibotenic酸 (1.0 microg/0.2 microL) 被神经化学损伤。NRM或网状核巨囊细胞/旁囊细胞复合物的神经元损伤降低了发作后的镇痛作用。同样,在其他独立组中,在研究的所有发作期后,与对照组相比,将利坦色林 (5.0 microg/0.2 microL) 或生理盐水集中施用到每个研究的网状形成核中,引起抓住动物的TFL在统计学上显着降低。这些结果表明,脑桥和延髓网状核的5-羟色胺输入连接的神经元可能参与了发作期后的镇痛。

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