Katsuura G, Arimura A, Koves K, Gottschall P E
U.S.-Japan Biomedical Research Laboratories, Tulane University Hebert Center, Belle Chasse 70037.
Am J Physiol. 1990 Jan;258(1 Pt 1):E163-71. doi: 10.1152/ajpendo.1990.258.1.E163.
Intravenous administration of recombinant human interleukin 1 beta (IL-1 beta, 1 micrograms/100 g body wt) resulted in a marked elevation of plasma adrenocorticotropic hormone (ACTH) levels, with peak levels at 10 min, in conscious unrestrained rats. One week after the placement of a lesion by radiofrequency or microinjection of kainic acid in the organum vasculosum of lamina terminalis (OVLT) but not in subfornical organ, ACTH response to intravenous IL-1 beta was enhanced, whereas both radiofrequency-induced lesion and kainic acid in the preoptic area (POA) suppressed the response. Indomethacin or a prostaglandin E (PGE) antagonist microinjected into the OVLT or POA suppressed or abolished the response. On the other hand, PGE, but not PGD2, microinjected into the POA increased plasma ACTH levels. These results suggest an important role for the OVLT, which lacks blood-brain barrier, as a possible site of entry of blood-borne IL-1 beta into the brain and for the POA, which may contain the neurons required for the response. Involvement of PGE in the OVLT and POA in the ACTH response to intravenous IL-1 beta is also suggested.
给清醒自由活动的大鼠静脉注射重组人白细胞介素1β（IL-1β，1微克/100克体重），导致血浆促肾上腺皮质激素（ACTH）水平显著升高，在10分钟时达到峰值。在终板血管器（OVLT）而非穹窿下器通过射频或微量注射 kainic 酸造成损伤一周后，ACTH 对静脉注射IL-1β的反应增强，而视前区（POA）的射频诱导损伤和 kainic 酸均抑制了该反应。向OVLT或POA微量注射吲哚美辛或前列腺素E（PGE）拮抗剂可抑制或消除该反应。另一方面，向POA微量注射PGE而非PGD2可提高血浆ACTH水平。这些结果表明，缺乏血脑屏障的OVLT作为血源性IL-1β进入大脑的可能部位以及可能包含该反应所需神经元的POA具有重要作用。还提示PGE参与了OVLT和POA对静脉注射IL-1β的ACTH反应。
