Prepulse inhibition (PPI) of tactile startle response in recombinant congenic strains of mice:QTL mapping and comparison with acoustic PPI

Prepulse inhibition （PPI） of the startle response is a psychophysiological measure of sensorimotor gating believed to be cross-modal between different sensory systems. We analyzed the tactile startle response （TSR） and PPI of TSR （tPPI）, using light as a prepulse stimulus, in the mouse strains A/J and C57BL/6J and 36 recombinant congenic strains derived from them. Parental strains were significantly different for TSR, but were comparable for tPPI. Among the congenic strains, variation for TSR was significant in both genetic backgrounds, but that of tPPI was significant only for the C57BL/6J background. Provisional mapping for loci modulating TSR and tPPI was carried out. Using mapping data from our previous study on acoustic startle responses （ASR） and PPI of ASR （aPPI）, no common markers for aPPI and tPPI were identified. However, some markers were significantly associated with both ASR and TSR, at least in one genetic background. These results indicate cross-modal genetic regulation for the startle response but not for PPI, in these mouse strains.

Impaired prepulse inhibition of acoustic startle in Chinese patients with first-episode, medication-naive schizophrenia

Background Patients with schizophrenia have prominent abnormality in information processing that can be observed by measures of prepulse inhibition （PPI） of acoustic startle reflex and PPI deficits have been considered as a candidate endophenotypic marker of schizophrenia. However, there has been little information on PPI and related measures in Chinese patients with schizophrenia. The research was to explore the deficits of acoustic startle reflex that might exist in Chinese patients with schizophrenia. Methods Startle response to acoustic stimuli, habituation, and PPI were examined in 31 Chinese patients with first-episode, medication-naive schizophrenia and 30 age-and sex-matched healthy Chinese controls. At the same day of startle testing, psychopathological symptoms of the patients were assessed with the Positive and Negative Syndrome Scale （PANSS）. Results Compared with healthy controls, patients exhibited the significant reduction in startle response and PPI deficits at 60 milliseconds （ms） intervals （PP160, P 〈0.05） but not at 30 or 120 ms intervals. Furthermore, there was a relatively strong correlation between PPI60 （P 〈0.05） and scores of positive scale of PANSS in patients with schizophrenia. Conclusion Our findings confirmed impaired PPI in Chinese patients with schizophrenia and suggested that a relationship between sensorimotor gating deficits and clinical symptoms of patients with schizophrenia might exist.

Chronic morphine treatment decreases acoustic startle response and prepulse inhibition in rats

The reward-related effects of addictive drugs primarily act via the dopamine system, which also plays an important role in sensorimotor gating. The mesolimbic dopamine system is the common pathway of drug addiction and sensorimotor gating. However, the way in which addictive drugs affect sensorimotor gating is currently unclear. In previous studies, we examined the effects of morphine treatment on sensory gating in the hippocampus. The present study investigated the effects of morphine on sensorimotor gating in rats during chronic morphine treatment and withdrawal. Rats were examined during treatment with morphine for 10 successive days, followed by a withdrawal period. Acoustic startle responses to a single startle stimulus (115 dB SPL) and prepulse inhibition responses were recorded. The results showed that acoustic startle responses were attenuated during morphine treatment, but not during withdrawal. PPI was impaired in the last 2 morphine treatment days, but returned to a normal level during withdrawal.

惊跳反射前脉冲抑制在听觉领域的研究进展

惊跳反射前脉冲抑制(prepulse inhibition,PPI)是一种复杂的听觉行为反应,为评估人类和实验动物的听觉门控系统提供了有价值的方法。其神经通路涉及中枢听觉皮层,因此对于探究动物及人类(尤其是婴幼儿)听觉皮层的发育变化具有重要意义。本文对PPI在听觉科学领域近年来的研究进行总结,并探讨今后的发展趋势。

间隙前抑制耳后肌反射应用于小型猪模型

目的 应用小型猪作为研究对象,分别应用耳后肌反射(Post-Auricular Muscle Response, PAMR)与眨眼反射(Eye-Blink Response, EBR)测量间隙前抑制惊跳反射(Gap-induced inhibition of the Acoustic Startle, GPIAS),从而确定PAMR可成为测量GPIAS的方法,为耳鸣模型验证提供更加敏感、客观的方法。方法 选取3只3月龄大小的雄性小猪,分别应用PAMR以及EBR进行5次耳鸣模型行为范式—GPIAS的检测。应用SPSS21.0软件进行统计分析。结果 每只小型猪PAMR在no-gap情况下幅值均大于给予gap时的情况;每只小型猪EBR“no-gap”幅值大于“gap”时,但多数无统计学意义,且出现了gap幅值大于no-gap幅值的情况;进行GN Ratio(gap/no-gap)的计算后比较发现PAMR的ratio值均稳定小于1,EBR的值波动较大且出现>1的情况。结论 PAMR可以稳定且客观地反映耳鸣行为学检测范式GPIAS,表明PAMR可以成为小型猪耳鸣动物模型检测的方法,为后续阐明耳鸣的机制奠定了基础。

大鼠听觉发育中听觉敏感度及时间分辨率的变化

目的运用听觉惊跳反射前抑制方法观察大鼠听觉系统发育过程中听觉敏感度和时间分辨率的改变及两者之间的时间相关性。方法选用日龄为14、16、18、22、26、30、35天的新生SD大鼠各20只,各日龄大鼠分为2组,每组10只,每个日龄组的大鼠均进行听性脑干反应（ABR）测试和听觉惊跳反射前抑制测试,一组大鼠在测试时标记的背景噪声频率为1~48 kHz,另一组大鼠的背景噪声频率为8~32 kHz。结果 1、2和4 kHz ABR阈值在第26天、16和32 kHz ABR阈值在第22天、8和48 kHz ABR阈值在第18天与第35天比较差异无统计学意义（P〉0.05）。因此,生后第26天,大鼠听觉系统各频率已发育完全,听敏度已达到正常成年大鼠的水平。听觉惊跳反射前抑制测试表明当背景噪声为8~32 kHz时,第14天大鼠的间隔阈值为50 ms左右;第16、18、22、26天大鼠的间隔阈值为25 ms;第30天大鼠的间隔阈值为15 ms;第35天大鼠的间隔阈值为8 ms。当背景噪声为1~48 kHz时,间隔阈值明显下降（P=0.013）,第14天大鼠的间隔阈值为25 ms;第16、18天大鼠的间隔阈值为15ms;第22、26、30、35天大鼠的间隔阈值为10 ms。但在两种背景噪声下,时间分辨率均在第30天发育成熟。结论在大鼠听觉系统发育过程中,时间分辨率的发育落后于听敏度的发育。

间歇前抑制惊跳反射在听觉科学领域的研究进展

间歇前抑制惊跳反射(gap prepulse inhibition of acoustic startle response,GPIAS)是一种有效且便捷的评估动物听觉系统乃至相关神经系统的客观测试方法,目前常用于听觉领域和精神疾病的研究。它来自于动物的先天性反射行为,不需要提前训练,因此测试结果具有较好的稳定性和可靠性。本文对该测试技术的背景、影响因素及听觉系统相关应用进行综述。

单次延长应激对大鼠惊跳反射和弱刺激抑制的影响

目的初步探讨单次延长应激后大鼠惊跳反射和弱刺激抑制变化情况。方法60只SD大鼠按随机数字表法分为6组，阴性对照1，7，14d组，应激1，7，14d组，每组10只大鼠。阴性对照组不接受任何处理，应激组接受单次延长应激。阴性对照1d组和应激1d组、阴性对照7d组和应激7d组、阴性对照14d组和应激14d组分别在在应激后第2，8，15天接受惊跳反射和弱刺激抑制测试。结果阴性对照1，7，14d组惊跳反射和弱刺激抑制实验结果之间差异无统计学意义（P〉0．05）。应激1d组惊跳反射[（92．49±31．54）g，P〈0．05]高于阴性对照1d组[（64．48±17．95）g]，但其弱刺激抑制[（28．60±29．02）％，P〈0．05]低于阴性对照1d组[（41．60±15．10）％]；应激7d组和阴性对照7d组惊跳反射结果差异无统计学意义（P〉0．05），应激7d组弱刺激抑制[（17．95±31．79）％，P〈0．05]低于阴性对照7d组[（41．30±12．79）％]；应激14d组和阴性对照14d组惊跳反射结果差异没有统计学意义（P〉0．05），应激14d组弱刺激抑制[（13．71±32．48）％，P〈0．05]低于阴性对照14d组[（41．16±12．25）％]。结论大鼠凉跳反射的增加存在于应激后早期，而弱刺激抑制的损害在应激后早期出现，并在应激后持续较长时间。

震惊反射系统在研究小鼠感觉运动门控功能中的应用

感觉运动门控功能异常与多种精神疾病相关,前脉冲抑制是常用的测量感觉运动门控的重要行为学参数。该文介绍了用震惊反射系统测定C57BL/6J品系小鼠前脉冲抑制的实验方法,并用N-甲基-D-天冬氨酸受体非竞争拮抗剂MK-801(Dizocilpine,地卓西平)成功构建了药物诱发前脉冲抑制缺失的小鼠模型。