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在暴露于急性疼痛时,CA1海马区中D1样和D2样多巴胺受体在应激诱导的抗伤害感受反应中的作用。

Role of D1- and D2-like dopamine receptors within the CA1 hippocampal region in the stress-induced antinociceptive response in the exposure to acute pain.

作者信息

Shirmohammadi Diba, Golmohammadi Homayoon, Seyedaghamiri Fatemehsadat, Haghparast Abbas

机构信息

School of Medicine, Iran University of Medical Sciences.

Neuroscience Research Center, School of Medicine, Shahid Beheshti University of Medical Sciences.

出版信息

Behav Pharmacol. 2025 Feb 1;36(1):30-39. doi: 10.1097/FBP.0000000000000810. Epub 2024 Dec 24.

Abstract

Exposure to stressful conditions such as forced swim stress (FSS) induces antinociception. Previous reports determined that dopamine receptors in the CA1 hippocampal area are important in chronic pain processing. Considering that neural mechanisms behind acute and chronic pain differ significantly, in this study, we have investigated the role of dopamine receptors within the CA1 region in the FSS-induced antinociceptive response in the acute pain induced by the tail-flick test in the rat. The cannula was implanted unilaterally in the CA1 region of the animal brain. Animals received drugs or vehicles 5 min before FSS exposure. SCH23390 as the D1-like dopamine receptor (D1R) antagonist and Sulpiride as the D2-like dopamine receptor (D2R) antagonist were microinjected into the CA1 area at three doses (0.25, 1, and 4 μg/0.5 μl vehicle); the vehicle groups received saline instead of SCH23390 and dimethyl sulfoxide instead of Sulpiride. After exposure to FSS, the tail-flick test was done. The findings of this study revealed that FSS significantly attenuates nociceptive response during the tail-flick test ( P  < 0.0001). Moreover, intra-CA1 microinjection of SCH23390 and Sulpiride significantly reduces the FSS-induced antinociception in the inducing acute pain ( P  < 0.0001). The comparison of effective dose of 50% for D1R and D2R antagonists showed that both receptors in the CA1 almost equally reduce the FSS-induced antinociception in the tail-flick test. The result of this study supports the hypothesis, that the dopaminergic system in CA1 is involved in triggering a stress-induced antinociceptive response in acute pain conditions.

摘要

暴露于诸如强迫游泳应激(FSS)等应激条件会诱发抗伤害感受。先前的报道表明,海马CA1区的多巴胺受体在慢性疼痛处理中起重要作用。鉴于急性和慢性疼痛背后的神经机制存在显著差异,在本研究中,我们调查了CA1区域内多巴胺受体在FSS诱导的大鼠甩尾试验急性疼痛抗伤害感受反应中的作用。将套管单侧植入动物脑的CA1区域。动物在暴露于FSS前5分钟接受药物或赋形剂。将作为D1样多巴胺受体(D1R)拮抗剂的SCH23390和作为D2样多巴胺受体(D2R)拮抗剂的舒必利以三种剂量(0.25、1和4μg/0.5μl赋形剂)微量注射到CA1区域;赋形剂组接受生理盐水而非SCH23390,接受二甲亚砜而非舒必利。暴露于FSS后,进行甩尾试验。本研究结果表明,FSS在甩尾试验期间显著减弱伤害感受反应(P < 0.0001)。此外,CA1区内微量注射SCH23390和舒必利显著降低了FSS诱导的急性疼痛抗伤害感受(P < 0.0001)。D1R和D2R拮抗剂50%有效剂量的比较表明,CA1区的两种受体在甩尾试验中几乎同等程度地降低了FSS诱导的抗伤害感受。本研究结果支持以下假设,即CA1区的多巴胺能系统参与在急性疼痛条件下触发应激诱导的抗伤害感受反应。

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