Publications by authors named "Anda van Stegeren"

Background: Research suggests that yohimbine hydrochloride (YOH), a noradrenaline agonist, can facilitate fear extinction. It is thought that the mechanism of enhanced emotional memory is stimulated through elevated noradrenaline levels. This randomized placebo-controlled trial examined the potential exposure-enhancing effects of YOH in a clinical sample of participants meeting DSM-IV criteria for a specific phobia (fear of flying).

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Stress is known to differentially modulate memory function. Memory can be impaired or strengthened by stress, depending on e.g.

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Emotional stimuli may prime the motor system and facilitate action readiness. Direct evidence for this effect has been shown by recent studies using transcranial magnetic stimulation (TMS). When administered over the primary motor cortex involved in responding, TMS pulses elicit motor-evoked potentials (MEPs) in the represented muscles.

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Emotionally arousing experiences are usually well retained, an effect that depends on the release of adrenal stress hormones. Animal studies have shown that corticosterone and noradrenaline - representing the two main stress hormone systems - act in concert to enhance memory formation by actions involving the amygdala, hippocampus and prefrontal cortex (PFC). Here we test whether interactions between these two stress hormone systems also affect human memory formation as well as the associated pattern of brain activation.

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Objective: To review and give an overview of neuroimaging studies that look at the role of stress (hormones) on memory.

Method: An overview will be given of imaging studies that looked at the role of stress (hormones) on memory. Stress is here defined as the acute provocation of the sympathetic adrenal medullar system and the hypothalamic-pituitary-adrenal axis in experimental designs.

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Neuro-endocrine markers such as salivary alpha amylase (sAA) and cortisol (CORT) play an important role in establishing human responses to stressful events. Whereas sAA levels reflect sympathetic system activity, salivary cortisol appears to be a valid measure for HPA axis activity. Although many studies looked at either sAA or CORT responses in reaction to stress, work still has to be done to look at the way these systems interact, especially when both systems are activated.

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This contribution is an overview on the role of noradrenaline as neurotransmitter and stress hormone in emotional memory processing. The role of stress hormones in memory formation of healthy subjects can bear significance for the derailment of memory processes, for example, in post traumatic stress disorder (PTSD). Increased noradrenaline levels lead to better memory performance, whereas blocking the noradrenergic receptors with a betablocker attenuates this enhanced memory for emotional information.

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Animal studies show that glucocorticoid effects on memory depend on noradrenergic activation within an intact amygdala. Testing this model in humans is the subject of the present fMRI study. Healthy subjects watched emotional and neutral stimuli after having received a betablocker or placebo.

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Animal studies show that high cortisol levels exert their effect on stressful task performance via modulation of the amygdala. Availability of noradrenaline in this brain region appears to be a critical prerequisite for this effect. This relationship between noradrenaline and cortisol is explained by an animal model where the amygdala constitutes a crucial region for this interaction.

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Free salivary cortisol is an established non-invasive marker of hypothalamus pituitary adrenal (HPA) axis activity. In contrast, such a well-characterized salivary marker for activity of the sympatho-adrenal medullar (SAM) system is still missing. As one potential candidate salivary alpha amylase (sAA) has been suggested.

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The amygdala is a pivotal structure in humans for encoding of emotional information, as shown by recent imaging studies. It is unknown which neurotransmitters are specifically involved in the human amygdala, although in animal studies noradrenaline was shown to be essential. In our study, participants received the betablocker propranolol (which blocks the noradrenergic response) or placebo when watching neutral to highly negative arousing pictures.

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On the basis of recent evidence indicating a sex-related lateralization of amygdala function in memory for emotional events, together with substantial evidence suggesting hemispheric specialization in processing global (central) versus local (detail) aspects of a situation, and the established dependence of the amygdala's memory modulating function on beta-adrenergic receptor activation, we predicted differential effects of a beta-adrenergic receptor antagonist (propranolol) on long-term memory for an emotionally arousing story in men and women. Specifically, we predicted that, relative to placebo, propranolol would impair memory for information central to the story line, but not memory for peripheral story details in men. Conversely, propranolol would impair memory for peripheral details, but not for central information in women.

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Rationale: Animal and human studies lend support to the hypothesis that enhanced memory associated with emotional experiences involves activation of the beta-adrenergic system. Evidence for the role of noradrenaline in emotional memory in humans has been gathered from experimental studies where blockade of the beta-adrenergic system with a beta-blocker selectively impaired long-term memory for an emotionally arousing story (a slide show), when the beta-blocker was given before subjects were confronted with the emotional stimuli.

Objective: The purpose of this study was to test whether effective beta-adrenergic blockade occurring only after the stage of encoding has a similar impairing effect on memory.

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