The modulating role of ADRA2B in emotional working memory: Attending the negative but remembering the positive

Aging and the genetic road towards the positivity effect in memory

“…Here, we will focus on the following polymorphisms (see Box 1 for a Glossary): (1) a deletion variant of the ADRA2B gene, which influences activity of adrenergic receptors; (2) the single nucleotide polymorphism Val/Met in the COMT gene, involved in prefrontal dopamine metabolism; (3) a short allele of the 5HTTLPR serotonin transporter gene. Previous studies reported that these three polymorphisms can modulate information processing in regions involved in emotional memories (e.g., the hippocampus, the amygdala and the PFC cortex (see Todd et al, 2011), and play an essential role in emotion and cognition interaction (Mammarella et al, 2016a). Mammarella et al (2016b) showed how genetic variants involved in noradrenergic signaling may contribute to age-related differences in emotional memory.…”

“…adrenoceptor gene (ADRA2B) has been recently linked to emotional memory (e.g., Mammarella et al, 2016a). The ADRA2B deletion reduces receptor functionality and increases central noradrenergic transmission, through the presynaptic inhibition of NA release.…”

“…Behaviorally, deletion carriers show enhanced memory for emotional material due to an emotional arousal-induced activation of noradrenergic neurotransmission (see Todd et al, 2011). A series of behavioral studies, in fact, have found that deletion carriers tend to show a general arousal enhancement effect in long-term memory tasks (see Mammarella et al, 2016a). fMRI data also suggests that deletion carriers exhibit increased neural activity in the amygdala during encoding of emotional pictures (Rasch et al, 2009).…”

ADRA2B deletion variant influences time-dependent effects of pre-learning stress on long-term memory

“…Previous work has shown that the ADRA2B deletion variant is associated with enhanced emotional memory, heightened amygdala responses to emotional stimuli and greater intrusiveness of traumatic memories (Cousijn et al, 2010; de Quervain et al, 2007; Li et al, 2015; Mammarella et al, 2016; Rasch et al, 2009; Todd et al, 2013). We have extended this area of research by demonstrating that the ADRA2B deletion variant influences pre-learning stress effects on long-term memory in a time- and sex-dependent manner.…”

“…Although this variant is associated with both agonistic and antagonistic effects in vitro (Small, Brown, Forbes, and Liggett, 2001), researchers have speculated that it results in greater norepinephrine availability during emotional events (Rasch, Spalek, Buholzer, Luechinger, Boesiger, Papassotiropoulos, and de Quervain, 2009), a physiological condition associated with enhanced learning and memory (McGaugh, 2004). In healthy individuals, carriers of the ADRA2B deletion variant exhibit enhanced perception and memory of emotional stimuli (de Quervain, Kolassa, Ertl, Onyut, Neuner, Elbert, and Papassotiropoulos, 2007; Mammarella, Fairfield, Di Domenico, D’Onofrio, Stuppia, and Gatta, 2016; Todd, Muller, Lee, Robertson, Eaton, Freeman, Palombo, Levine, and Anderson, 2013), as well as greater amygdala activity during the encoding of emotionally arousing information (Cousijn, Rijpkema, Qin, van Marle, Franke, Hermans, van Wingen, and Fernandez, 2010; Rasch et al, 2009), which, in some cases, has been selectively reported following stress (Li, Weerda, Milde, Wolf, and Thiel, 2015). Although there are no studies showing a greater incidence of PTSD in deletion carriers, research has shown that the deletion variant is associated with greater intrusiveness of traumatic memories in Rwandan Civil War survivors (de Quervain et al, 2007), and the significant amount of work revealing exaggerated noradrenergic activity in PTSD (Skelton et al, 2012; Strawn and Geracioti, 2008; Zoladz and Diamond, 2013) presents the possibility of a connection between the ADRA2B deletion variant and PTSD-like phenotypes that warrants further investigation.…”