苯环利定和阿扑吗啡诱导的大鼠惊吓闸门缺陷的个体发生。
Ontogeny of phencyclidine and apomorphine-induced startle gating deficits in rats.
作者信息
Martinez Z A, Halim N D, Oostwegel J L, Geyer M A, Swerdlow N R
机构信息
Department of Psychology, University of California, Los Angeles, CA, USA.
出版信息
Pharmacol Biochem Behav. 2000 Mar;65(3):449-57. doi: 10.1016/s0091-3057(99)00217-8.
NMDA antagonists and dopamine (DA) agonists produce neuropathological and/or behavioral changes in rats that may model specific abnormalities in schizophrenia patients. In adult rats, NMDA antagonists and DA agonists disrupt sensorimotor gating-measured by prepulse inhibition (PPI)-modeling PPI deficits in schizophrenia patients. In addition, high doses of NMDA antagonists produce limbic system pathology that may model neuropathology in schizophrenia patients. We examined these behavioral and neuropathological models across development in rats. Both the NMDA antagonist phencyclidine (PCP) and the DA agonist apomorphine disrupted PPI in 16 day pups, demonstrating early developmental functionality in substrates regulating these drug effects on PPI. In contrast, PCP neurotoxicity was evident only in adult rats. Brain mechanisms responsible for the PCP disruption of PPI, and PCP-induced neurotoxicity, are dissociable across development.
N-甲基-D-天冬氨酸（NMDA）拮抗剂和多巴胺（DA）激动剂会在大鼠身上产生神经病理学和/或行为变化，这些变化可能模拟精神分裂症患者的特定异常情况。在成年大鼠中，NMDA拮抗剂和DA激动剂会破坏感觉运动门控——通过前脉冲抑制（PPI）来测量——模拟精神分裂症患者的PPI缺陷。此外，高剂量的NMDA拮抗剂会产生边缘系统病理学变化，这可能模拟精神分裂症患者的神经病理学。我们在大鼠发育过程中研究了这些行为和神经病理学模型。NMDA拮抗剂苯环利定（PCP）和DA激动剂阿扑吗啡均破坏了16日龄幼崽的PPI，表明在调节这些药物对PPI作用的底物中存在早期发育功能。相比之下，PCP神经毒性仅在成年大鼠中明显。负责PCP对PPI的破坏以及PCP诱导的神经毒性的脑机制在整个发育过程中是可分离的。
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