Nisticó G, Caroleo M C, Arbitrio M, Pulvirenti L
Department of Biology, University of Rome Tor Vergata, Italy.
Neuroimmunomodulation. 1994 May-Jun;1(3):174-80. doi: 10.1159/000097158.
Indirect evidence suggests that dopamine within the brain may participate in the regulation of immune responses both in humans and in rodents. The aim of the present study was to investigate the possible modulatory role played by specific dopamine D1 receptor subtypes within discrete sites of the brain dopaminergic pathways. Mitogen responsiveness of splenocytes and natural killer (NK) cell activity were measured in rats following microinfusion of SKF 38393, a specific dopamine D1 receptor agonist, into the ventral tegmental area, the amygdala, the nucleus accumbens and the CA1 area of the hippocampus. We report here that microinfusion of SKF 38393 (100 nmol) within the central amygdala increased the proliferative response of splenocytes to concanavalin A (ConA) while it did not modify the proliferative response of splenocytes to lipopolysaccharide (LPS) or NK cell activity. On the contrary, microinfusion of SKF 38393 into the nucleus accumbens decreased the proliferative response of splenocytes to ConA and LPS, while NK cell activity remained unchanged. Similarly, microinfusion of SKF 38393 into the CA1 area of the hippocampus decreased the proliferative response of splenocytes to LPS, but not to ConA and did not affect NK cell activity. Finally, microinfusion of SKF 38393 into the ventral tegmental area did not significantly modify the proliferative response of splenocytes to either ConA or LPS and did not affect NK cell activity. All immunological changes evoked through the different areas of the brain following microinfusion of SKF 38393 were prevented by systemic administration of SCH 23390, a specific D1 receptor antagonist.
间接证据表明，大脑中的多巴胺可能参与人类和啮齿动物免疫反应的调节。本研究的目的是探讨大脑多巴胺能通路离散部位特定多巴胺D1受体亚型可能发挥的调节作用。在将特异性多巴胺D1受体激动剂SKF 38393微量注入大鼠腹侧被盖区、杏仁核、伏隔核和海马CA1区后，测量脾细胞的丝裂原反应性和自然杀伤（NK）细胞活性。我们在此报告，在中央杏仁核内微量注入SKF 38393（100 nmol）可增加脾细胞对伴刀豆球蛋白A（ConA）的增殖反应，而不改变脾细胞对脂多糖（LPS）的增殖反应或NK细胞活性。相反，将SKF 38393微量注入伏隔核可降低脾细胞对ConA和LPS的增殖反应，而NK细胞活性保持不变。同样，将SKF 38393微量注入海马CA1区可降低脾细胞对LPS的增殖反应，但对ConA无影响，且不影响NK细胞活性。最后，将SKF 38393微量注入腹侧被盖区对脾细胞对ConA或LPS的增殖反应均无显著影响，也不影响NK细胞活性。通过微量注入SKF 38393后大脑不同区域引起的所有免疫变化，均可被特异性D1受体拮抗剂SCH 23390的全身给药所阻断。
