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Cocaine induced T cell proliferation in the rat: role of amygdala dopamine D1 receptors.

机译:可卡因诱导大鼠T细胞增殖:杏仁核多巴胺D1受体的作用。

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摘要

The immunomodulatory effects of local administration of cocaine into the amygdala were studied in the rat. Intra-amygdala infusion of cocaine significantly and dose-dependently increased the proliferative response of splenocytes to concanavalin A (Con A). A similar effect on the immune response was also observed in rats, microinfused into the central amygdala with the selective D1 receptor agonist SKF 38393. The increase of the proliferative response of splenocytes to Con A was inhibited by coinfusion within the central amygdala of the dopamine D1 receptor antagonist SCH 23390, together with cocaine, but not by coinfusion of the dopamine D2 receptor antagonist eticlopride. These results suggest that cocaine may produce at least some of its effects on the immune system through the activation of brain dopamine neurotransmission and that the central amygdala may represent a critical structure mediating cocaine-induced T cell proliferation.
机译:在大鼠中研究了将可卡因局部施用于杏仁核的免疫调节作用。杏仁内可卡因输注显着且剂量依赖性地增加了脾细胞对伴刀豆球蛋白A(Con A)的增殖反应。在大鼠中也观察到了类似的免疫反应效果,将其与选择性D1受体激动剂SKF 38393微输注到中央杏仁核中。在多巴胺D1中央杏仁核中共融合抑制了脾细胞对Con A增殖反应的增加。受体拮抗剂SCH 23390与可卡因一起使用,但不能通过多巴胺D2受体拮抗剂依替普利的共融合来实现。这些结果表明,可卡因可能通过激活脑多巴胺神经传递而对免疫系统产生至少一些影响,并且中央杏仁核可能代表介导可卡因诱导的T细胞增殖的关键结构。

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