Levine A S, Morley J E
Pharmacol Biochem Behav. 1981 Nov;15(5):735-8. doi: 10.1016/0091-3057(81)90014-9.
Intracerebroventricular administration of PGF2 alpha and PGE2 suppressed food intake in several feeding models. PGF2 alpha (20 micrograms) and PGE2 (20 micrograms to 1 micrograms) suppressed food intake following a 24 hour starvation. PGF2 alpha (20 micrograms) and PGE2 (20 micrograms) suppressed food intake following central administration of the feeding induces norepinephrine and muscimol. These prostaglandins also suppressed stress induced eating using the tail pinch model at doses of 20 micrograms, 10 micrograms and 5 micrograms with eating returning to control levels at the 1 micrograms dose. D-Ala Methionine Enkephalin failed to alter the suppressive effects of PGF2 alpha and PGE2 at a dose of 1 microgram but successfully reversed the effect of PGF2 alpha at a 10 micrograms dose while still having no effect on PGE2 suppression of feeding.
在多种进食模型中,脑室内注射前列腺素F2α(PGF2α)和前列腺素E2(PGE2)可抑制食物摄入。在24小时饥饿后,PGF2α(20微克)和PGE2(20微克至1微克)可抑制食物摄入。在中枢给予诱发进食的去甲肾上腺素和蝇蕈醇后,PGF2α(20微克)和PGE2(20微克)可抑制食物摄入。这些前列腺素在剂量为20微克、10微克和5微克时,使用夹尾模型也可抑制应激诱导的进食,在1微克剂量时进食恢复到对照水平。D-丙氨酸甲硫氨酸脑啡肽在1微克剂量时未能改变PGF2α和PGE2的抑制作用,但在10微克剂量时成功逆转了PGF2α的作用,而对PGE2抑制进食仍无影响。