تاثیر هورمونهای استرس بر حافظه هیجانی: ارتباط برای آسیب شناسی روانی

Substantial progress within recent years has led to a better understanding of the impact of stress on emotional memory. These effects are of relevance for understanding and treating psychopathology. The present selective review describes how emotional memory is modulated through stress hormones. Acute as well as chronic effects are discussed and information from rodent models is compared to human experimental studies and clinical observations. Finally, the relevance of these findings for emotional memory disturbances in psychiatric disorders is exemplified by discussions on neuroendocrine alterations in depression, post traumatic stress disorder and phobias.

Most psychiatric disorders are characterized by emotional memory or emotional learning disturbances. Brain regions involved in these processes are the two medial temporal lobe structures, amygdala and hippocampus, and several brain regions within the prefrontal cortex (PFC; LaBar & Cabeza, 2006). These learning and memory alterations are not just secondary symptoms but are key components of these disorders. For example, PTSD patients experience vivid flashbacks in which they relive the trauma (Nemeroff et al., 2006 and Rauch et al., 2006; see also Holmes & Bourne, 2008). Patients with major depression in contrast have a memory bias with a preferred storage and retrieval of negative information (Leppanen, 2006). Finally phobic patients display an exaggerated conditioned fear response which they cannot control cognitively (Centonze, Siracusano, Calabresi, & Bernardi, 2005). The examples illustrate that emotional memory dysfunctions appears to underlie several psychiatric disorders. In this context, actions of neuroendocrine stress mediators are of relevance. The goal of the present review is thus to highlight the influence of stress hormones on emotional memory and emotional learning. Starting from a basic science perspective, experimental work on animals and humans will be reviewed. Afterwards potential clinical implications are outlined using depression, PTSD and phobias as examples. Two systems will be considered: The hormones of the sympathetic nervous system (SNS; adrenalin and noradrenalin) and the hormones of the hypothalamus pituitary adrenal (HPA) axis (CRH, ACTH, and cortisol/corticosterone). These stress responsive systems interact at multiple levels in the periphery and the brain. Together they influence emotional memory in a complex manner.

The review has highlighted some of the recent advances in the field of stress hormone induced memory modulation. For acute stress the effects of stress depend on the memory domain and on the memory phase studied (encoding, consolidation, and retrieval). In addition, the effects are modulated by specifics of the learning material (e.g. the emotional arousal induced by it). Also important to note is that for some memory domains sex differences have been detected. For chronic stress effects the findings indicate structural alterations in the hippocampus and PFC, which are associated with impaired memory. However, in the amygdala, hypertrophy occurs and amygdala mediated forms of learning are enhanced, suggesting that a shift from PFC and hippocampal-based ‘cognitive’ learning towards an amygdala-based ‘affective’ learning occurs. Since these observations are mostly based on data obtained in animals, more human studies combining structural and functional neuroimaging with neuroendocrine measures are warranted. In the last part of the review, it was illustrated how these basic science findings might help to enhance our understanding of several psychiatric disorders. A modulation of emotional memory and emotional learning by stress hormones appears to be of relevance for the aetiology and/or for the treatment of depression, PTSD and phobias. Thus the last decade has seen substantial progress in this exciting area and the future looks even more promising. A more thorough neuroendocrine diagnostic work-up in combination with new drugs or specific psychotherapies targeted at specific neuroendocrine circuits in the brain should lead to an enhanced treatment success for several psychiatric disorders.