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高能重粒子辐射与小鼠惊吓反应及前脉冲抑制的多巴胺能修饰

HZE radiation and dopaminergic modification of startle and prepulse inhibition in mice.

作者信息

Haerich Paul, Nelson Gregory A, Pecaut Michael J

机构信息

NeuroCognition and Brain Studies Section, Department of Psychology, School of Science and Technology, Loma Linda University and Medical Center, CA 92350, USA.

出版信息

Physiol Behav. 2005 Sep 15;86(1-2):103-10. doi: 10.1016/j.physbeh.2005.06.024.

Abstract

C57BL/6 mice were exposed to 5 Gy (28)Si or (56)Fe particle radiation in order to explore the immediate or short-latency effect of exposure to high energy (HZE) particle radiation on dopaminergic modification of acoustic startle and prepulse inhibition. The radiation is representative of the type which would be encountered as galactic cosmic rays during long-duration space flight. The acoustic startle response was elicited with 120 dB white noise and prepulse inhibition of the startle response was produced with 79 dB and 86 dB stimuli presented with a 125 ms onset asynchrony. Startle reactivity was inhibited by (56)Fe radiation but not by (28)Si particles. Apomorphine (3 mg/kg) produced a general inhibition of startle reactivity while haloperidol (1 mg/kg) facilitated it. Apomorphine disrupted prepulse inhibition, but only in animals which were not exposed to radiation. Both (56)Fe and (28)Si radiation exposure attenuated the disruption of prepulse inhibition induced by apomorphine. In contrast, the facilitation of prepulse inhibition induced by haloperidol was not modified by radiation. These data are consistent with a short-latency disruption of dopaminergic systems by HZE particle radiation. We speculate that this disruption may occur as a restriction in the capacity of the dopaminergic system.

摘要

为了探究暴露于高能(HZE)粒子辐射对听觉惊吓和前脉冲抑制的多巴胺能修饰的即时或短潜伏期影响,将C57BL/6小鼠暴露于5 Gy的(28)硅或(56)铁粒子辐射下。这种辐射代表了在长时间太空飞行中作为银河宇宙射线可能遇到的类型。用120 dB白噪声引发听觉惊吓反应,并用79 dB和86 dB刺激以125 ms的起始异步呈现来产生惊吓反应的前脉冲抑制。惊吓反应性受到(56)铁辐射的抑制,但不受(28)硅粒子的抑制。阿扑吗啡(3 mg/kg)对惊吓反应性产生普遍抑制,而氟哌啶醇(1 mg/kg)则促进惊吓反应性。阿扑吗啡破坏了前脉冲抑制,但仅在未暴露于辐射的动物中。(56)铁和(28)硅辐射暴露均减弱了阿扑吗啡诱导的前脉冲抑制破坏。相比之下,氟哌啶醇诱导的前脉冲抑制促进作用不受辐射影响。这些数据与HZE粒子辐射对多巴胺能系统的短潜伏期破坏一致。我们推测这种破坏可能是由于多巴胺能系统能力受限而发生的。

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