ژنوتیپ ADRA2B اثرات استرس حاد روانی در حافظه هیجانی در مردان جوان سالم را تعدیل می کند
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|34453||2013||8 صفحه PDF||سفارش دهید||6969 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Neurobiology of Learning and Memory, Volume 103, July 2013, Pages 11–18
Previous studies have shown that acute psychosocial stress impairs retrieval of declarative memory with emotional material being especially sensitive to this effect. A functional deletion variant of the ADRA2B gene encoding the α2B-adrenergic receptor has been shown to increase emotional memory and neural activity in the amygdala. We investigated the effects of acute psychosocial stress and the ADRA2B allele on recognition memory for emotional and neutral faces. Fourty-two healthy, non-smoker male volunteers (30 deletion carriers, 12 noncarriers) were tested with a face recognition paradigm. During encoding they were presented with emotional and neutral faces. One hour later, participants underwent either a stress (“Trier Social Stress Test (TSST)”) or a control procedure which was followed immediately by the retrieval session where subjects had to indicate whether the presented face was old or new. Stress increased salivary cortisol concentrations, blood pressure and pulse and impaired recognition memory for faces independent of emotional valence and genotype. Participants showed generally slower reaction times to emotional faces. Carriers of the ADRA2B functional deletion variant showed an impaired recognition and slower retrieval of neutral faces under stress. Further, they were significantly slower in retrieving fearful faces in the control condition. The findings indicate that a genetic variation of the noradrenergic system may preserve emotional faces from stress-induced memory impairments seen for neutral faces and heighten reactivity to emotional stimuli under control conditions.
Acute psychosocial stress triggers a fast response inducing the release of noradrenaline and a slow response inducing the release of glucocorticoids. In humans, it has been shown that elevated levels of glucocorticoids impact on a variety of cognitive functions, especially learning and memory (reviewed in (Lupien, Maheu, Tu, Fiocco, & Schramek, 2007)). This influence depends critically on the timing of the stressor relative to the memory phase (Schwabe, Wolf, & Oitzl, 2010). Acute stress or administration of stress hormones before memory encoding improves later retrieval while administration of stress or stress hormones before retrieval often impairs performance (reviewed in (Wolf, 2008). For example, rats showed impaired spatial long-term memory when receiving a footshock prior to retention. This stress induced deficit could be abolished by blocking corticosterone synthesis (de Quervain, Roozendaal, & McGaugh, 1998). In humans, several studies provide evidence for impairments of memory when the stressor is applied prior to retrieval (Kuhlmann et al., 2005 and Tollenaar et al., 2008). Impairments were mainly demonstrated in tasks using verbal material and free recall (Buchanan et al., 2006 and Smeets et al., 2008). The stress-induced impairments are in line with the finding that pharmacological enhancement of glucocorticoid levels prior to retrieval reduced cued recall of word pairs learned 24 h earlier and decreased neural activity in the medial temporal lobe (de Quervain et al., 2003). Emotional memory is especially prone to acute psychosocial stress. In humans, emotional memory has often been studied by using emotional and neutral verbal material which volunteers had to recall 24 h later. Using such an approach, Kuhlmann et al. (2005) and Smeets et al. (2008)Smeets (2011) provide evidence that the stress induced impairment of verbal memory retrieval is stronger for emotional than for neutral words. Stress induced memory impairments are however also evident with shorter delays between encoding and retrieval. Buchanan and colleagues found stress-induced impairments in free recall of moderately arousing words 1 h after encoding. Similar impairments were reported by Merz et al. for socially relevant information (Buchanan et al., 2006 and Merz et al., 2010). Several studies investigated the interaction between glucocorticoids and noradrenaline with respect to encoding of emotional memories. These findings suggest that an interaction of these two endogenous modulators impacts on neural activity in hippocampus and amygdala, increasing memory for emotional items (Kukolja et al., 2011 and van Stegeren et al., 2010). Whether changes in noradrenergic activity also impact on retrieval of emotional memories is less well understood. While some studies, like (Tollenaar, Elzinga, Spinhoven, & Everaerd, 2009) did not find any evidence for impaired memory after blockade of noradrenergic activity with propanolol prior to retrieval, others found that the drug reduced retrieval of emotional material, an effect which was still evident 24 h later in the absence of the drug (Kroes, Strange, & Dolan, 2010). de Quervain, Aerni, et al., 2007 and de Quervain, Kolassa, et al., 2007 further investigated the interaction of propranolol administration and acute stress on recall of emotionally arousing words. They found that noradrenergic blockade alone did not affect recall of emotional or neutral words, but prevented the impairment of emotional memory induced by cortisone treatment. Additional evidence for a role of noradrenaline in emotional memory comes from genetic studies. A functional deletion variant of the ADRA2B gene which is characterised by a loss of three glutamic acid residues (301–303) in the third intracellular loop encoding the α2B subunit of the noradrenaline receptor, acts as a loss-of-function variant and increases noradrenaline availability. Behaviorally it has been shown that deletion carriers have enhanced memory for emotional pictures and it was suggested that this effect is due to an emotional arousal-induced activation of noradrenergic neurotransmission ( de Quervain, Aerni, et al., 2007 and de Quervain, Kolassa, et al., 2007). fMRI data suggest that deletion carriers exhibit increased neural activity in the amygdala during encoding of emotional pictures ( Rasch et al., 2009). Further, acute stress induced by showing short movie clips with highly aversive content, increased phasic amygdala responses to dynamically morphing emotional faces in deletion carriers but not in non-carriers. This suggests that stress modulates amygdala processing in a genotype specific way ( Cousijn et al., 2010). However, whether acute stress shows different effects on emotional memory as a function of ADRA2B receptor polymorphism is still unknown. The present study aimed to investigate whether acute psychosocial stress differentially impacts on recognition of neutral and emotional material as a function of ADRA2B genotype. Participants performed a recognition memory task for neutral and negative emotional faces and were exposed to the Trier Social Stress Test (TSST) ( Kirschbaum, Pirke, & Hellhammer, 1993) prior to memory retrieval. We expected to find impaired memory retrieval after stress, especially with respect to emotional faces. Further, we expected a genotype specific modulation of memory retrieval.