Molecular Cognition Laboratory, Department of Psychology, University of California, San Diego, CA 92093-0109, USA.
Neurosci Lett. 2010 Jan 1;468(1):18-22. doi: 10.1016/j.neulet.2009.10.049. Epub 2009 Oct 21.
Much research is focused on developing novel drugs to improve memory. In particular, psychostimulants have been shown to enhance memory and have a long history of safe use in humans. In prior work, we have shown that very low doses of amphetamine administered before training on a Pavlovian fear-conditioning task can dramatically facilitate the acquisition of cued fear. The current experiment sought to expand these findings to the extinction of cued fear, a well-known paradigm with therapeutic implications for learned phobias and post-traumatic stress disorder. If extinction reflects new learning, one might expect drugs that enhance the acquisition of cued fear to also enhance the extinction of cued fear. This experiment examined whether 0.005 or 0.05 mg/kg of D-amphetamine (therapeutic doses shown to enhance acquisition) also enhance the extinction of cued fear. Contrary to our hypothesis, amphetamine did not accelerate extinction. Thus, at doses that enhance acquisition of conditioned fear, amphetamine does not appear to enhance extinction.
许多研究都集中在开发新型药物以改善记忆。特别是,精神兴奋剂已被证明可以增强记忆,并且在人类中安全使用已有很长的历史。在之前的工作中,我们已经表明,在进行条件性恐惧训练之前给予非常低剂量的安非他命可以极大地促进条件性恐惧的获得。当前的实验旨在将这些发现扩展到条件性恐惧的消退,这是一种具有治疗学习恐惧症和创伤后应激障碍的著名范例。如果消退反映了新的学习,那么人们可能会期望增强条件性恐惧获得的药物也会增强条件性恐惧的消退。本实验检查了 0.005 或 0.05mg/kg 的 D-安非他命(已显示出可增强获得的治疗剂量)是否也可增强条件性恐惧的消退。与我们的假设相反,安非他命并没有加速消退。因此,在增强条件性恐惧获得的剂量下,安非他命似乎不会增强消退。