The Amygdala Modulates the Consolidation of Memories of Emotionally Arousing Experiences

Abstract

Converging findings of animal and human studies provide compelling evidence that the amygdala is critically involved in enabling us to acquire and retain lasting memories of emotional experiences. This review focuses primarily on the findings of research investigating the role of the amygdala in modulating the consolidation of long-term memories. Considerable evidence from animal studies investigating the effects of posttraining systemic or intra-amygdala infusions of hormones and drugs, as well as selective lesions of specific amygdala nuclei, indicates that (a) the amygdala mediates the memory-modulating effects of adrenal stress hormones and several classes of neurotransmitters; (b) the effects are selectively mediated by the basolateral complex of the amygdala (BLA); (c) the influences involve interactions of several neuromodulatory systems within the BLA that converge in influencing noradrenergic and muscarinic cholinergic activation; (d) the BLA modulates memory consolidation via efferents to other brain regions, including the caudate nucleus, nucleus accumbens, and cortex; and (e) the BLA modulates the consolidation of memory of many different kinds of information. The findings of human brain imaging studies are consistent with those of animal studies in suggesting that activation of the amygdala influences the consolidation of long-term memory; the degree of activation of the amygdala by emotional arousal during encoding of emotionally arousing material (either pleasant or unpleasant) correlates highly with subsequent recall. The activation of neuromodulatory systems affecting the BLA and its projections to other brain regions involved in processing different kinds of information plays a key role in enabling emotionally significant experiences to be well remembered.

The role of biomarkers and MEG-based imaging markers in the diagnosis of post-traumatic stress disorder and blast-induced mild traumatic brain injury

“…Hyporesponsive PFC, as well as reduced connectivity to the amygdala (Jin et al, 2013;Shin et al, 2004a) may indicate insufficient inhibitory control over exaggerated fear responses. Lastly, abnormal hippocampal function (Corcoran and Maren, 2001) and reduced connectivity to the amygdala (Dolcos et al, 2004;McGaugh, 2004) may underlie impairments in contextual memory processing and the ability to inhibit intrusive memories (Shin et al, 2004a), although findings have been mixed (Hughes and Shin, 2011). A recent resting-state fMRI study showed increased activity in amygdala and reduced spontaneous neural activity in the dorso-lateral PFC (DLPFC) (Yan et al, 2013).…”

Inhibition of learning and memory by general anesthetics

“…[35][36][37][38][39][40][41] In addition, the amygdala modulates fear-related learning in other brain structures, such as the cortex and hippocampus. [42][43][44][45] Some types of fear conditioning, including the contextual and trace fear conditioning, also involve the hippocampus. [46][47][48][49][50][51] Unlike the hippocampus, the amygdala is necessary for the acquisition of fearful memories and their long-term storage and retrieval.…”

Memory modulation in the classroom: Selective enhancement of college examination performance by arousal induced after lecture

“…Importantly, emotional and arousing events are known to be better recollected than neutral events, which is thought due at least in part to the influence of neural and hormonal responses to such events (LaBar & Cabeza, 2006;McGaugh, 2000McGaugh, , 2004. Specifically, stressful and arousing events cause increased release of substances such as glucose, cortisol, and epinephrine (Dickerson & Kemeny, 2004;McCarty & Gold, 1981;McGaugh, 1990McGaugh, , 2000Merali, McIntosh, Kent, Michaud, & Anisman, 1998;Piazza & Le Moal, 1997), which have been repeatedly associated with memory modulation (e.g., Czech, Nielson, & Laubmeier, 2000;LaBar & Cabeza, 2006;McGaugh, 2000;Nielson, Czech, & Laubmeier, 1999;Nielson & Jensen, 1994;van Stegeren, Everaerd, Cahill, McGaugh, & Gooren, 1998).…”

“…Specifically, stressful and arousing events cause increased release of substances such as glucose, cortisol, and epinephrine (Dickerson & Kemeny, 2004;McCarty & Gold, 1981;McGaugh, 1990McGaugh, , 2000Merali, McIntosh, Kent, Michaud, & Anisman, 1998;Piazza & Le Moal, 1997), which have been repeatedly associated with memory modulation (e.g., Czech, Nielson, & Laubmeier, 2000;LaBar & Cabeza, 2006;McGaugh, 2000;Nielson, Czech, & Laubmeier, 1999;Nielson & Jensen, 1994;van Stegeren, Everaerd, Cahill, McGaugh, & Gooren, 1998). These substances act, at least in part, by influencing amygdala function, which then modulates the memory consolidation processes (Adolphs, Tranel, & Buchanan, 2005;Canli, Zhao, Brewer, Gabrieli, & Cahill, 2000;Kensinger & Corkin, 2004;McGaugh, 2004). Importantly, memory modulatory effects can be generated during or after learning.…”

“…Alternatively, studies in animal models and humans have suggested that post-learning arousal manipulations initiate a series of neuromodulatory mechanisms that enhance the consolidation of the recently learned material (cf. McGaugh, 2000McGaugh, , 2004. Whether these mechanisms lead to increased rumination or whether these may be parallel and complementary mechanisms remains to be clarified in future research.…”