Autobiographisches Gedächtnis, der Einfluss von frühkindlichem Stress und neuronalen Korrelaten

Vandekerckhove M. Autobiographical memory begins and ends with the self : autobiographical memory, consciousness, the influence of stress and neural correlates. Bielefeld (Germany): Bielefeld University; 2004.The general purpose of this thesis is to study some fundamental, yet still open questions about autobiographical memory and related consciousness, the influence of early stress on the brain and autobiographical memory and its neural correlates. The goal is to make some progress in the definitory confusion and conceptual understanding of the relationship of these concepts starting from a developmental point of view. In the attempt to throw some light on what can fall under the sum of autobiographical memory-related themes, no overview or review of the existing answers will be given but rather, after extended research of the theoretical and empirical literature and own empirical work, a new clarifying point of view of the different phenomena. Considering the close relationship between the experience of the world, consciousness and autobiographical memory, the first question that becomes addressed in the theoretical part is how a child develops autobiographical memory and what Tulving entitles as associated "autonoetic consciousness", a self-reflective mental state of awareness in time and space (Tulving, 1985; 2002). The second question is concerned with how early childhood can form the basal template in the buffering and facilitation of influences of stress on the brain and also on autobiographical memory, with psychogenic amnesia and altered autonoetic consciousness as a prototypical example. Autobiographical old memories are as a result of a high degree of anatomical interconnectivity and cognitive complexity most vulnerable to brain damage and other external and internal influences such as stress (Markowitsch, 1995; 1999; 2000; 2002; 2003; Tulving and Markowitsch, 1998). The second empirical part of the thesis is primarily focused on the fundamental research of autobiographic memory and its neural correlates. The different focuses within the chapters will bring up more questions for theoretical thinking and empirical research about the same complexity of which individuals are made of

Olfaction, Emtion & the Amygdala: arousal-dependent modulation of long-term autobiographical memory and its association with olfaction

The sense of smell is set apart from other sensory modalities. Odours possess the capacity to trigger immediately strong emotional memories. Moreover, odorous stimuli provide a higher degree of memory retention than other sensory stimuli. Odour perception, even in its most elemental form - olfaction - already involves limbic structures. This early involvement is not paralleled in other sensory modalities. Bearing in mind the considerable connectivity with limbic structures, and the fact that an activation of the amygdala is capable of instantaneously evoking emotions and facilitating the encoding of memories, it is unsurprising that the sense of smell has its characteristic nature. The aim of this review is to analyse current understanding of higher olfactory information processing as it relates to the ability of odours to spontaneously cue highly vivid, affectively toned, and often very old autobiographical memories (episodes known anecdotally as Proust phenomena). Particular emphasis is placed on the diversity of functions attributed to the amygdala. Its role in modulating the encoding and retrieval of long-term memory is investigated with reference to lesion, electrophysiological, immediate early gene, and functional imaging studies in both rodents and humans. Additionally, the influence of hormonal modulation and the adrenergic system on emotional memory storage is outlined. I finish by proposing a schematic of some of the critical neural pathways that underlie the odour-associated encoding and retrieval of emotionally toned autobiographical memories

Episodic memory for emotional information: Event-related potential and functional magnetic resonance imaging studies

The neural correlates of emotional episodic memory are investigated in a series of neuroimaging experiments (ERP, fMRI) through the comparison of memory effects elicited during retrieval of emotional relative to neutral information. In the first two ERP studies, it is revealed that emotionally-valenced words influence recognition memory primarily by virtue of their high levels of 'semantic-cohesiveness'. Furthermore, the findings reveal that the arrangement of emotional and neutral retrieval cues at test (blocked versus intermixed) influences processing carried out upon retrieved emotional episodic information. The findings across the third and fourth ERP studies indicate that incidental retrieval of emotional context (encoding environment) gives rise to greater activity in neural systems supporting episodic retrieval than does retrieval of non-emotional context. When context retrieval is intentional, by contrast, emotional and non-emotional episodic memory are associated with equivalent levels of engagement. The findings of the fourth ERP study are consistent with the existence of additional neural circuitry that is activated selectively by emotionally toned episodic information. In a final event-related fMRI study it is revealed that the retrieval of emotionally negative relative to emotionally neutral context elicits enhanced activity in brain regions including prefrontal cortex, amygdala, hippocampus and retrosplenial cortex. Recognition of words from positive relative to neutral contexts is associated with increased activity in prefrontal and orbitofrontal cortex, and in the left anterior temporal lobe. The fMRI findings provide further support for the proposal that the incidental retrieval of emotional information enhances activity in networks supporting episodic retrieval of neutral information. In addition, the fMRI findings suggest that regions known to be activated when emotional information is encountered in the environment are also active when emotional information is retrieved from memory. Whilst the findings are noteworthy in their own right, they also have implications for future studies of emotional memory. It is proposed that the employment of paradigms which involve the retrieval of emotional context through presentation of non-emotional retrieval cues may offer advantages over paradigms wherein the retrieval cues themselves are emotional

Neural activity associated with episodic memory for emotional context

To address the question of which brain regions subserve retrieval of emotionally-valenced memories, we used event-related fMRI to index neural activity during the incidental retrieval of emotional and non-emotional contextual information. At study, emotionally neutral words were presented in the context of sentences that were either negatively, neutrally or positively valenced. At test, fMRI data were obtained while participants discriminated between studied and unstudied words. Recognition of words presented in emotionally negative relative to emotionally neutral contexts was associated with enhanced activity in right dorsolateral prefrontal cortex, left amygdala and hippocampus, right lingual gyrus and posterior cingulate cortex. Recognition of words from positive relative to neutral contexts was associated with increased activity in bilateral prefrontal and orbitofrontal cortices, and left anterior temporal lobe. These findings suggest that neural activity mediating episodic retrieval of contextual information and its subsequent processing is modulated by emotion in at least two ways. First, there is enhancement of activity in networks supporting episodic retrieval of neutral information. Second, regions known to be activated when emotional information is encountered in the environment are also active when emotional information is retrieved from memory. Copyright © 2001 Elsevier Science Ltd

True and False Memories: Neuropsychological and Neuropharmacological Approaches

Some recent studies have explored the false memory and its mechanisms. True memories depend on draw in the past, retrieve of the information, remember past events plus recombine (reorganize) them with new information to finally re-encode these elements creating a new memory. But, sometimes failures in this system lead to memory errors collaborating to false memory formation. This chapter will address new neuropsychological tools to evaluate true and false memory performance. Some neuropharmacological aspects as possible mechanisms of agonist and antagonist modulation of false memory will be discussed

Memory Reconsolidation Mediates the Updating of Hippocampal Memory Content

The retrieval or reactivation of a memory places it into a labile state, requiring a process of reconsolidation to restabilize it. This retrieval-induced plasticity is a potential mechanism for the modification of the existing memory. Following previous data supportive of a functional role for memory reconsolidation in the modification of memory strength, here I show that hippocampal memory reconsolidation also supports the updating of contextual memory content. Using a procedure that separates the learning of pure context from footshock-motivated contextual fear learning, I demonstrate doubly dissociable hippocampal mechanisms of initial context learning and subsequent updating of the neutral contextual representation to incorporate the footshock. Contextual memory consolidation was dependent upon BDNF expression in the dorsal hippocampus, whereas the footshock modification of the contextual representation required the expression of Zif268. These mechanisms match those previously shown to be selectively involved in hippocampal memory consolidation and reconsolidation, respectively. Moreover, memory reactivation is a necessary step in modifying memory content, as inhibition of hippocampal synaptic protein degradation also prevented the footshock-mediated memory modification. Finally, dorsal hippocampal knockdown of Zif268 impaired the reconsolidation of the pure contextual memory only under conditions of weak context memory training, as well as failing to disrupt contextual freezing when a strong contextual fear memory is reactivated by further conditioning. Therefore, an adaptive function of the reactivation and reconsolidation process is to enable the updating of memory content

The Modulatory Influences of Amygdala-Hippocampal Interactions on Emotional Memory

This thesis is a literature review on the effects that emotion has on memory. The influences that emotion has on memory will be analyzed, specifically through the lens of amygdala-hippocampal interactions. Primary focus will be on the compilation and analysis of emotional memory studies, and how the enhancement of emotional memories is facilitated by amygdala-hippocampal modulation. By viewing brain activity and the direct or indirect projections to and from these specific brain regions, I will provide a cohesive, critical literature review of relevant cognitive neuroscience work on emotional memory and amygdala-hippocampus connections. By compiling relevant cognitive neuroscience findings in one thesis, this will make it easier to understand and comprehend the amygdala-hippocampal interconnection and its impact on emotional memory

Cocaine Diminishes Consolidation of Cued Fear Expression in Female Rats Through Interactions With Dopamine D2 Receptors

In addition to cocaine’s addictive properties, cocaine use may lead to heightened risk-taking behaviors in individuals despite potentially aversive consequences. One possible reason for this may be cocaine’s disruptive effect on aversive memory formation. The present study investigated the effects of cocaine on fear memory formation using a cued fear conditioning paradigm in female Sprague Dawley rats. On day 1, animals received tone-shock pairings and on day 2 (24 hours later) were returned to the fear chamber and tested for recall of fear memory. Fear was measured as percent time the animal spent freezing during the tone presentation. In Experiment 1 (n = 48), cocaine (15mg/kg; i.p.) was administered prior to or immediately after the conditioning trials to assess the effect of cocaine on fear memory acquisition and consolidation. To determine whether cocaine’s effects on memory consolidation are mediated by D2 receptors, the D2 receptor antagonist eticlopride (0.1mg/kg; i.p.) was administered concurrently with cocaine. No drugs were administered on test day. Results from Experiment 1 revealed that pre-training cocaine diminishes fear acquisition and that post-conditioning cocaine resulted in diminished fear expression during fear test. Concurrent D2 antagonism attenuated the impairing effect of cocaine on fear memory consolidation, with animals showing increased freezing relative to animals receiving cocaine alone. In Experiment 2 (n = 15), animals received direct infusions of eticlopride (0.05 μl/min) into the ventral hippocampus (VH), a structure known to be involved in cued fear conditioning and a target region of ventral tegmental area, substantia nigra, and locus coeruleus dopaminergic neurons. Intra-VH eticlopride or saline was directly infused into the VH immediately after conditioning concurrent to cocaine administration. Results from Experiment 2 suggest that the antagonism of VH D2 receptors may disrupt the impairing effects of cocaine on fear memory consolidation, suggesting the VH as a potential region mediating this effect. The present study provides evidence that acute cocaine administration impairs aversive memory formation and establishes a potential circuit through which cocaine induces its detrimental effects on fear memory consolidation. Moreover, these results provide insight into why cocaine users might engage in impulsive and risk-taking behavior that could lead to fatal consequences

Active Forgetting: Adaptation of Memory by Prefrontal Control.

Over the past century, psychologists have discussed whether forgetting might arise from active mechanisms that promote memory loss to achieve various functions, such as minimizing errors, facilitating learning, or regulating one's emotional state. The past decade has witnessed a great expansion in knowledge about the brain mechanisms underlying active forgetting in its varying forms. A core discovery concerns the role of the prefrontal cortex in exerting top-down control over mnemonic activity in the hippocampus and other brain structures, often via inhibitory control. New findings reveal that such processes not only induce forgetting of specific memories but also can suppress the operation of mnemonic processes more broadly, triggering windows of anterograde and retrograde amnesia in healthy people. Recent work extends active forgetting to nonhuman animals, presaging the development of a multilevel mechanistic account that spans the cognitive, systems, network, and even cellular levels. This work reveals how organisms adapt their memories to their cognitive and emotional goals and has implications for understanding vulnerability to psychiatric disorders

Opposing effects of negative emotion on amygdalar and hippocampal memory for items and associations

Although negative emotion can strengthen memory of an event it can also result in memory disturbances, as in post-traumatic stress disorder (PTSD). We examined the effects of negative item content on amygdalar and hippocampal function in memory for the items themselves and for the associations between them. During fMRI, we examined encoding and retrieval of paired associates made up of all four combinations of neutral and negative images. At test, participants were cued with an image and, if recognised, had to retrieve the associated (target) image. The presence of negative images increased item memory but reduced associative memory. At encoding, subsequent item recognition correlated with amygdala activity, while subsequent associative memory correlated with hippocampal activity. Hippocampal activity was reduced by the presence of negative images, during encoding and correct associative retrieval. In contrast, amygdala activity increased for correctly retrieved negative images, even when cued by a neutral image. Our findings support a dual representation account, whereby negative emotion up-regulates the amygdala to strengthen item memory but down-regulates the hippocampus to weaken associative representations. These results have implications for the development and treatment of clinical disorders in which diminished associations between emotional stimuli and their context contribute to negative symptoms, as in PTSD