Org 2766可防止NMDA受体拮抗剂破坏前庭代偿。
Org 2766 prevents disruption of vestibular compensation by an NMDA receptor antagonist.
作者信息
Gilchrist D, Darlington C, Smith P
机构信息
Department of Psychology, University of Otago, Dunedin, New Zealand.
出版信息
Eur J Pharmacol. 1994 Jan 24;252(1):R1-2. doi: 10.1016/0014-2999(94)90584-3.
The adrenocorticotrophic hormone fragment 4-9 (ACTH-(4-9)) analog, Org 2766 has been shown to accelerate vestibular compensation. However, N-methyl-D-aspartate (NMDA) receptor antagonists disrupt the recovery process. When Org 2766 was administered at a dose of 20 nmol/kg every 4 h for 52 h, it prevented the disruption of compensation usually produced by a single 5 mg/kg i.p. injection of the NMDA receptor antagonist 3-([+]-2-carboxy-piperazin-4yl)-propyl-1-phosphonic acid (CPP). NMDA receptor antagonists and ACTH-like peptides may produce their effects on compensation by acting directly or indirectly at the same receptor complex.
促肾上腺皮质激素片段4-9（ACTH-(4-9)）类似物Org 2766已被证明可加速前庭代偿。然而，N-甲基-D-天冬氨酸（NMDA）受体拮抗剂会干扰恢复过程。当以每4小时20 nmol/kg的剂量给予Org 2766，持续52小时时，它可防止通常由单次腹腔注射5 mg/kg的NMDA受体拮抗剂3-([+]-2-羧基-哌嗪-4基)-丙基-1-膦酸（CPP）所产生的代偿干扰。NMDA受体拮抗剂和ACTH样肽可能通过直接或间接作用于同一受体复合物而对代偿产生影响。
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