Laboratory of Behavioural Neurobiology, Swiss Federal Institute of Technology Zurich, Schorenstrasse 16, CH 8603 Schwerzenbach, Switzerland.
Pharmacol Biochem Behav. 2012 Mar;101(1):107-14. doi: 10.1016/j.pbb.2011.12.010. Epub 2011 Dec 21.
Prepulse inhibition (PPI) of the acoustic startle reflex refers to the reduction of the startle response to an intense acoustic pulse stimulus when it is shortly preceded by a weak non-startling prepulse stimulus and provides a cross-species measure of sensory-motor gating. PPI is typically impaired in schizophrenia patients, and a similar impairment can be induced in rats by systemic scopolamine, a muscarinic cholinergic receptor antagonist that can evoke a range of cognitive and psychotic symptoms in healthy humans that are commonly referred to as the "anti-muscarinic syndrome" resembling some clinical features of schizophrenia. Scopolamine-induced PPI disruption has therefore been proposed as an anti-muscarinic animal model of schizophrenia, but parallel investigations in the mouse remain scant and the outcomes are mixed and often confounded by an elevation of startle reactivity. Here, we distinguished the PPI-disruptive and the confounding startle-enhancing effects of scopolamine (1 and 10mg/kg, i.p.) in C57BL/6 wild-type mice by showing that the latter partly stemmed from a shift in spontaneous baseline reactivity. With appropriate correction for between-group differences in startle reactivity, we went on to confirm that the PPI-disruptive effect of scopolamine could be nullified by clozapine pre-treatment (1.5mg/kg, i.p.) in a dose-dependent manner. This is the first demonstration that scopolamine-induced PPI disruption is sensitive to atypical antipsychotic drugs. In concert with previous data showing its sensitivity to haloperidol the present finding supports the predictive validity of the anti-muscarinic PPI disruption model for both typical and atypical antipsychotic drug action.
声发射起始反射的前脉冲抑制(PPI)是指当强的声学脉冲刺激之前紧随一个弱的非起始刺激时,起始反射的减少,提供了一种跨物种的感觉运动门控测量方法。精神分裂症患者的 PPI 通常受损,而全身东莨菪碱(一种毒蕈碱型乙酰胆碱受体拮抗剂)可以在大鼠中诱导类似的损伤,东莨菪碱可以在健康人中引起一系列认知和精神病症状,通常被称为“抗毒蕈碱综合征”,类似于精神分裂症的一些临床特征。因此,东莨菪碱诱导的 PPI 破坏被提议作为精神分裂症的抗毒蕈碱动物模型,但在小鼠中的平行研究仍然很少,结果是混杂的,并且经常受到起始反应性升高的混淆。在这里,我们通过显示后者部分源自自发基线反应性的转变,区分了东莨菪碱(1 和 10mg/kg,ip)的 PPI 破坏和令人混淆的起始增强作用(1 和 10mg/kg,ip)。在适当校正起始反应性的组间差异后,我们继续确认,氯氮平预处理(1.5mg/kg,ip)可以以剂量依赖的方式消除东莨菪碱的 PPI 破坏作用。这是首次证明东莨菪碱诱导的 PPI 破坏对非典型抗精神病药物敏感。与先前显示其对氟哌啶醇敏感性的数据一致,本研究结果支持抗毒蕈碱 PPI 破坏模型对典型和非典型抗精神病药物作用的预测有效性。