Neural mechanisms of reconsolidation blockade in humans

重新巩固是指内存在重新激活后暂时变得不稳定的过程。最近的研究结果表明，β-肾上腺素能拮抗剂心得安可以阻碍再巩固，从而降低被认为是导致创伤后应激障碍症状的侵入性记忆的强度。然而，通过心得安介导情绪记忆再巩固的神经机制在很大程度上仍未被探索。本研究旨在缩小这一差距。厌恶记忆将使用恐惧条件反射范式建立。七天后，这些恐惧记忆将被重新激活，并使用心得安来阻止重新巩固。再过三天后，将测试恐惧条件反射，以调查心得安是否能够阻止再巩固。此外，还将评估心得安对再巩固的影响是否具有情境特异性。因变量包括使用功能磁共振成像测量的皮肤电导反应、心率、唾液皮质醇和神经激活变化。拟议项目的结果将阐明“降压药可能模糊坏记忆”的机制。点。, 2009)。

Reconsolidation refers to the process in which a memory is rendered transiently labile after its reactivation. Recent findings suggest that the β-adrenergic antagonist Propranolol can impede the reconsolidation and thus reduce the strength of intrusive memories believed to cause the symptomatology in Posttraumatic Stress Disorder. However, the neural mechanisms mediating the blockade of emotional memory reconsolidation through Propranolol remain largely unexplored. The present study aims to close this gap. Aversive memories will be established using a fear conditioning paradigm. Seven days later, these fear memories will be reactivated and Propranolol will be administered to block reconsolidation. After another three days, the fear conditioning will be tested to investigate if Propranolol was capable of blocking the reconsolidation. Furthermore, it will be assessed whether the Propranolol effect on reconsolidation is context-specific. Dependent variables include skin conductance responses, heart rate, salivary cortisol, and neural activation changes as measured using fMRI. The results of the proposed project will shed light on the mechanisms by which “a blood pressure drug may dim bad memories” (Sci. Am., 2009).