Stone E A, Rhee J, Quartermain D
Department of Psychiatry, New York University School of Medicine, NY 10016, USA.
Pharmacol Biochem Behav. 1996 Oct;55(2):215-7. doi: 10.1016/s0091-3057(96)00070-6.
Previous studies have shown that acute stress impairs risk assessment behavior in mice. The present study was undertaken to determine the role of beta adrenoceptors, which are known to be stimulated by stress, in this effect. Mice were treated with either a beta-1 antagonist, betaxolol, a beta-2 antagonist, ICI 118551, an alpha-1 antagonist, prazosin, or an alpha-2 antagonist, yohimbine, and 30 min later were subjected to a 1-h session of restraint stress. Thirty minutes after the stress the animals were tested for the entry latency, number of headpokes prior to entry, and the path of entry into a white open field from a small dark box. In agreement with previous findings, stress was found to markedly reduce risk assessment behaviors as reflected by a reduced entry latency, a reduced number of headpokes and a changed entry path from wall hugging to central entry. Betaxolol was found to prevent all of the above effects of stress dose dependently, whereas ICI 118551, prazosin, and yohimbine had no reversal effects. It is concluded that beta-1 receptor activation and possibly brain glycogen depletion is involved in the effects of stress on risk assessment behavior.
先前的研究表明，急性应激会损害小鼠的风险评估行为。本研究旨在确定已知会被应激激活的β肾上腺素能受体在这种效应中的作用。给小鼠分别注射β1拮抗剂倍他洛尔、β2拮抗剂ICI 118551、α1拮抗剂哌唑嗪或α2拮抗剂育亨宾，30分钟后对其进行1小时的束缚应激。应激30分钟后，测试动物进入潜伏期、进入前探头部次数以及从小暗箱进入白色开放场地的进入路径。与先前的研究结果一致，应激被发现显著降低了风险评估行为，表现为进入潜伏期缩短、探头部次数减少以及进入路径从贴壁进入变为中央进入。发现倍他洛尔能剂量依赖性地预防应激的上述所有效应，而ICI 118551、哌唑嗪和育亨宾没有逆转作用。结论是，β1受体激活以及可能的脑糖原耗竭参与了应激对风险评估行为的影响。
