Liminga U, Johansson P, Nylander I, Gunne L M
Psychiatric Research Centre, Uppsala, Sweden.
Psychopharmacology (Berl). 1989;99(3):299-303. doi: 10.1007/BF00445547.
Leu- and Metenkephalin (Lenk and Menk) and their more stable analogues D-Ala-Leu- and D-Ala-Metenkephalin (DALenk and DAMenk) as well as D-Ala-D-Leu- and D-Ala-D-Metenkephalin (DADLenk and DADMenk) were infused bilaterally into substantia nigra in awake rats and oral movements were recorded for 90 min. DADLenk and DADMenk elicited dose-dependent biting dyskinesias with a chewing rate of about 90 jaw movements/min. DALenk produced a similar but weaker effect, whereas DAMenk, Lenk and Menk were ineffective in the doses given. These findings suggest a possible enkephalinergic mechanism underlying neuroleptic-induced tardive dyskinesias.
亮氨酸脑啡肽和甲硫氨酸脑啡肽（Leu-脑啡肽和Met-脑啡肽）及其更稳定的类似物D-丙氨酸-亮氨酸脑啡肽和D-丙氨酸-甲硫氨酸脑啡肽（D-Ala-Leu-脑啡肽和D-Ala-Met-脑啡肽）以及D-丙氨酸-D-亮氨酸脑啡肽和D-丙氨酸-D-甲硫氨酸脑啡肽（D-Ala-D-Leu-脑啡肽和D-Ala-D-Met-脑啡肽）双侧注入清醒大鼠的黑质，并记录90分钟的口腔运动。D-Ala-D-Leu-脑啡肽和D-Ala-D-Met-脑啡肽引起剂量依赖性咬肌运动障碍，咀嚼频率约为每分钟90次下颌运动。D-Ala-Leu-脑啡肽产生类似但较弱的效果，而D-Ala-Met-脑啡肽、Leu-脑啡肽和Met-脑啡肽在所给剂量下无效。这些发现提示了抗精神病药物所致迟发性运动障碍潜在的脑啡肽能机制。
