Ontogeny of phencyclidine and apomorphine-induced startle gating deficits in rats

被引:38
作者
Martinez, ZA
Halim, ND
Oostwegel, JL
Geyer, MA
Swerdlow, NR
机构
[1] Univ Calif San Diego, Dept Psychiat, Sch Med, La Jolla, CA 92093 USA
[2] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90028 USA
[3] Univ Utrecht, Fac Pharm, Utrecht, Netherlands
关键词
apomorphine; development; neurotoxicity; phencyclidine; prepulse inhibition; schizophrenia; sensorimotor; startle;
D O I
10.1016/S0091-3057(99)00217-8
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
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. Nh IDA 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. (C) 2000 Elsevier Science Inc.
引用
收藏
页码:449 / 457
页数:9
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