The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law

Abstract

We have reviewed research on the effects of stress on LTP in the hippocampus, amygdala and prefrontal cortex (PFC) and present new findings which provide insight into how the attention and memory-related functions of these structures are influenced by strong emotionality. We have incorporated the stress-LTP findings into our “temporal dynamics” model, which provides a framework for understanding the neurobiological basis of flashbulb and traumatic memories, as well as stress-induced amnesia. An important feature of the model is the idea that endogenous mechanisms of plasticity in the hippocampus and amygdala are rapidly activated for a relatively short period of time by a strong emotional learning experience. Following this activational period, both structures undergo a state in which the induction of new plasticity is suppressed, which facilitates the memory consolidation process. We further propose that with the onset of strong emotionality, the hippocampus rapidly shifts from a “configural/cognitive map” mode to a “flashbulb memory” mode, which underlies the long-lasting, but fragmented, nature of traumatic memories. Finally, we have speculated on the significance of stress-LTP interactions in the context of the Yerkes-Dodson Law, a well-cited, but misunderstood, century-old principle which states that the relationship between arousal and behavioral performance can be linear or curvilinear, depending on the difficulty of the task.

The effect of communication skills training on residents’ physiological arousal in a breaking bad news simulated task

“…Their physiological arousal becomes probably more proportional to the complexity of the task and reflects cognitive and emotional activation to engage in the task and to respond with learned communication skills to task challenges. These results are similar with results of other studies that have shown a link between performance and arousal [24][25][26][27].…”

“…Moderate physiological arousal levels may therefore result in optimal performance, whereas too little or too much arousal may result in sub-optimal performances [23][24][25][26]. Physiological arousal levels have also been shown to be related to individuals' appraisal of their ability to perform a given task: when individuals perceive that they are unable to perform a complex task (threat appraisal), they may experience difficulties in engaging themselves in the task and their physiological arousal levels remain low, whereas when individuals perceive that they are able to perform a complex task, they experience less difficulties in engaging themselves in the task and their physiological arousal levels remain elevated (challenge appraisal) [26,27].…”

Association of Volume of Patient Encounters with Residents’ In-Training Examination Performance

“…This inverted U curve was described by Yerkes and Dodson, and is associated with the learning of difficult tasks. 13 In our study, there was a linear correlation in the IM PGY-2 year for the inpatient and subspecialty experiences, such that each additional 50 patient encounters was associated with an increase of 1 % correct on the ITE. The increase associated with the average of 263 patient encounters would be 5 % more correct on the ITE, which is consistent with the national average year-to-year increase in ITE score.…”

Effects of psychosocial stress on episodic memory updating

“…There appears to be a narrow range for optimal norepinephrine (Aston-Jones & Cohen, 2005) and dopamine activity in the PFC (Arnsten & Goldman-Rakic, 1998;Murphy, Arnsten, Goldman-Rakic, & Roth, 1996;Zahrt, Taylor, Mathew, &Arnsten, 1997). In addition, stress effects are rapid in the PFC (Diamond, Campbell, Park, Halonen, & Zoladz, 2007;Lupien, Gillin, & Hauger, 1999;Roozendaal, McReynolds, McGaugh, 2004) it is inhibited under high stress immediately, unlike the gradual hippocampal inhibition, and remains inhibited as long as stress hormones are secreted (Diamond, Campbell, Park, Halonen, & Zoladz, 2007).…”