Motivation and memory

心理学理论的一个基本原则是，行为是由记忆来指导的--对发生的事情的记忆，对我们对它们的感觉的记忆，对我们在哪里找到需要的东西的记忆，对什么与什么有关的记忆，以及对我们如何做事情的记忆，比如骑自行车或开车。并不是所有的记忆都对我们有帮助，对创伤事件的记忆或对令人愉悦的药物效应的记忆被认为保持病理性状态，如恐慌症或药物滥用。当代记忆理论认为，记忆存储在参与感知记忆事件的细胞之间的生化和结构变化中。这些变化被认为是相对永久性的，但最近有人提出，当记忆重新激活时，结构基础暂时变得可塑性，记忆可以通过干扰记忆存储的生化机制的处理来改变或破坏。目前尚不清楚这是否适用于所有类型的内存，或者这种中断是否是永久性的。我们有证据表明，在大鼠身上，被认为是导致吗啡成瘾的药物效应的记忆，可以被在非依赖动物表达对药物的动机时应用的记忆阻断药物打乱。然而，这种影响似乎是暂时的，并被一种新的药物体验所克服。此外，当动物依赖的时候，记忆似乎能抵抗干扰。这个项目的目的是探索改变剂量、使用一种以上的阻断药物或改变记忆阻断药物的应用时机是否会改善记忆障碍并使其永久存在。与此同时，我们将调查记忆是真的丢失了还是只是被抑制了。我们还将检查表明大脑中记忆的生化变化的解剖学标记，看看我们是否可以跟踪记忆阻断药物导致的记忆丧失。

It is a fundamental principle of psychological theory that behaviour is guided by memories - memories of things that happened and how we felt about them, memories of where we find the things we need, memories of what relates to what, and memories of how we do things like ride a bicycle or drive car. Not all memories are helpful to us, memories of traumatic events or memories of euphoric drug effects are thought to maintain pathological states such as panic disorder or drug abuse. Contemporary theories of memory hold that memories are stored in biochemical and structural changes in the connections between the cells that participate in the perception of the remembered events. These changes were thought to be relatively permanent but more recently it has been suggested that when memories are re-activated the structural basis becomes temporarily plastic and memories can be altered or disrupted by treatments that interfere with the biochemical mechanisms of memory storage. It is not known whether this applies to all types of memory, or whether the disruption is permanent or not. We have evidence in rats that the memories of drug effects that are thought drive morphine addiction can be disrupted by memory-blocking drugs applied around the time a non-dependent animal expresses his motivation for the drug. However this effect seems to be temporary and is overcome by a new experience of the drug. Also when the animal is dependent the memories appear to be resistant to disruption. The aim of this project is to explore whether changing the dose, using more than one blocking drug or changing the timing of application of the memory blocking drug will improve the amnesia and make it permanent. At the same time we will probe whether the memory is truly lost or just suppressed. We will also examine anatomical markers for the biochemical changes that indicate memory in the brain to see if we can track the loss of the memory induced by memory blocking drugs.