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首页> 外文期刊>The European Journal of Neuroscience >Angiotensin II modulates amphetamine-induced glial and brain vascular responses, and attention deficit via angiotensin type 1 receptor: Evidence from brain regional sensitivity to amphetamine
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Angiotensin II modulates amphetamine-induced glial and brain vascular responses, and attention deficit via angiotensin type 1 receptor: Evidence from brain regional sensitivity to amphetamine

机译：血管紧张素II通过血管紧张素类型1受体调节Amphetamine诱导的胶质和脑血管反应，并通过血管紧张素型受体的注意力缺陷：来自脑区域敏感性对安非他明的证据

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Amphetamine-induced neuroadaptations involve vascular damage, neuroinflammation, a hypo-functioning prefrontal cortex (PFC), and cognitive alterations. Brain angiotensin II, through angiotensin type 1 receptor (AT(1)-R), mediates oxidative/inflammatory responses, promoting endothelial dysfunction, neuronal oxidative damage and glial reactivity. The present work aims to unmask the role of AT(1)-R in the development of amphetamine-induced changes over glial and vascular components within PFC and hippocampus. Attention deficit was evaluated as a behavioral neuroadaptation induced by amphetamine. Brain microvessels were isolated to further evaluate vascular alterations after amphetamine exposure. Male Wistar rats were administered with AT(1)-R antagonist, candesartan, followed by repeated amphetamine. After one week drug-off period, animals received a saline or amphetamine challenge and were evaluated in behavioral tests. Afterward, their brains were processed for cresyl violet staining, CD11b (microglia marker), GFAP (astrocyte marker) or von Willebrand factor (vascular marker) immunohistochemistry, and oxidative/cellular stress determinations in brain microvessels. Statistical analysis was performed by using factorial ANOVA followed by Bonferroni or Tukey tests. Repeated amphetamine administration increased astroglial and microglial markers immunoreactivity, increased apoptotic cells, and promoted vascular network rearrangement at the PFC concomitantly with an attention deficit. Although the amphetamine challenge improved the attentional performance, it triggers detrimental effects probably because of the exacerbated malondialdehyde levels and increased heat shock protein 70 expression in microvessels. All observed amphetamine-induced alterations were prevented by the AT(1)-R blockade. Our results support the AT(1)-R involvement in the development of oxidative/inflammatory conditions triggered by amphetamine exposure, affecting cortical areas and increasing vascular susceptibility to future challenges.
机译：Amphetamine诱导的神经展开涉及血管损伤，神经炎性炎症，过逆转前额叶皮质（PFC）和认知改变。脑血管紧张素II，通过血管紧张素1受体（在（1）-R）中，介导氧化/炎症反应，促进内皮功能障碍，神经元氧化损伤和胶质反应性。目前的作品旨在揭示（1）-R在PFC和海马内胶质血管组分的胶质和血管组分的变化的发展中的作用。注重缺陷被评估为Amphetamine诱导的行为神经展示。分离脑微血管以进一步评估疗法暴露后的血管改变。雄性Wistar大鼠用（1）-R拮抗剂，糖果园施用，然后重复甜胺。经过一周的药物关闭，动物接受盐水或安非他明攻击，并在行为试验中进行评估。之后，将其大脑加工用于酸紫罗兰染色，CD11b（微胶质细胞标志物），GFAP（星形细胞标志物）或von Willebrand因子（血管标记）免疫组化，以及脑微血管中的氧化/细胞应激测定。通过使用因子Anova进行统计分析，然后进行Bonferroni或Tukey测试。重复的amphetamine给药增加了星形痛和微胶质标记物免疫反应性，增加的凋亡细胞，并伴随着注意力缺陷的PFC在PFC下促进了血管网络重排。虽然安非他明挑战提高了注意力的性能，但由于丙二醛水平加剧和微血管中的热休克蛋白70表达增加，它可能会触发有害影响。所有观察到的Amphetamine诱导的改变被AT（1）-R封闭。我们的结果支持（1）-R参与在由甜胺暴露引发的氧化/炎症条件的发展，影响皮质区域，增加对未来挑战的血管敏感性。

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