مسدود شدن آدرنرژیک بتا در طول فعال شدن مجدد احساس ذهنی یادآوری مرتبط با خاطرات اپیزودیک عاطفی را کاهش می دهد
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|33684||2013||6 صفحه PDF||سفارش دهید||4754 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Biological Psychology, Volume 92, Issue 2, February 2013, Pages 227–232
In contrast to neutral events, emotionally arousing events often are remembered vividly and with great detail. Although generally adaptive to survival, this emotional memory enhancement may contribute to psychopathology. Blocking the arousal-related noradrenergic activity with a β blocker shortly after learning prevents the emotional enhancement of memory. In the present experiment, we tested in 48 healthy subjects whether the administration of the β blocker propranolol before the reactivation of already consolidated emotional episodic memories may interfere with their reconsolidation and, thus, reduce the subsequent feeling of remembering associated with these memories. Our results show that propranolol before reactivation abolished the superior memory for emotional relative to neutral stimuli and decreased ‘remember’ judgments for emotional items, suggesting that β-adrenergic blockade during reactivation made emotional memories comparable to neutral memories.
Reactivating apparently stable, consolidated memories may render them unstable again, so that a process of reconsolidation is needed to stabilize them anew (Dudai, 2006, Lewis et al., 1968 and Nader and Hardt, 2009). During reconsolidation, memories can be updated by incorporating new experiences (Forcato et al., 2007, Hupbach et al., 2007 and Schiller et al., 2010) or modified by amnesic agents (Eisenberg and Dudai, 2004, Kindt et al., 2009 and Nader et al., 2000). Such reconsolidation manipulations provide an opportunity to alter unwanted memories and thus a pathological hallmark of several psychiatric disorders, including post-traumatic stress disorder (PTSD). The overly strong memory for traumatic events that is characteristic for PTSD (American Psychiatric Association, 1994) can be seen as an extreme form of the otherwise adaptive memory enhancement for emotional events. Emotionally arousing events are usually very well remembered and this emotional memory enhancement is mediated by noradrenergic activity in the amygdala (McGaugh, 2000 and Phelps and LeDoux, 2005). The overstimulation of endogenous stress hormone systems due to an extremely stressful event mediates an over-consolidation of the event, resulting in a lasting trauma memory (Pitman, 1989). Emotional arousal, however, leads not necessarily to memories that are particularly accurate (emotion may sometimes even increase false alarm rates; e.g. Johansson et al., 2004 and Kapucu et al., 2008) but rather to memories that are particularly vivid and associated with a strong subjective feeling of remembering (Ochsner, 2000, Sharot et al., 2004 and Talarico and Rubin, 2003). Most likely, it is this vividness, this subjective sense of remembering that makes memory so painful in PTSD. Blocking the arousal associated with emotional events by a β-adrenergic antagonist shortly after encoding prevents the emotional memory enhancement in healthy subjects (Cahill et al., 1994) and may reduce the risk for PTSD in individuals that have experienced a potentially traumatic event (Pitman et al., 2002). Although these data are promising, their clinical applicability may be limited as these effects are confined to a relatively short window after an event has happened (Ji et al., 2003), during which most people will not receive a clinical treatment. However, if reactivated memories are sensitive to similar manipulations as new memories, β-adrenergic blockade after memory reactivation should affect the reconsolidation of emotional memories and, thus, abolish the emotional memory enhancement a considerable time after the original memory was created. Support for this idea comes from rodent and human studies showing that β-adrenergic blockade during the reactivation of a conditioned fear may reduce the subsequent fear memory (Debiec and LeDoux, 2004, Kindt et al., 2009 and Soeter and Kindt, 2011). In the present experiment, we hypothesized that the administration of the β-adrenergic antagonist propranolol before memory reactivation would reduce the subjective feeling of remembering associated with emotional episodic memories. We used the ‘remember/know’ procedure to assess the subjective sense of remembering neutral and emotionally arousing episodic memories. Participants were asked to indicate whether a previously presented stimulus evokes specific, vivid memories of its occurrence (‘remembering’) or whether they cannot recollect any specific aspects of its presentation (‘knowing’). According to the dual-process theory of recognition memory (Yonelinas, 2002), ‘remembering’ and ‘knowing’ reflect two distinct processes that engage separable neural networks (Henson et al., 1999 and Wheeler and Buckner, 2004). In particular, the amygdala, which processes emotional arousal (Kensinger and Corkin, 2004), is implicated in ‘remembering’ but not in ‘knowing’ emotional stimuli (Sharot et al., 2004).