Awake Reactivation of Prior Experiences Consolidates Memories and Biases Cognition.

After experiences are encoded into memory, post-encoding reactivation mechanisms have been proposed to mediate long-term memory stabilization and transformation. Spontaneous reactivation of hippocampal representations, together with hippocampal-cortical interactions, are leading candidate mechanisms for promoting systems-level memory strengthening and reorganization. While the replay of spatial representations has been extensively studied in rodents, here we review recent fMRI work that provides evidence for spontaneous reactivation of nonspatial, episodic event representations in the human hippocampus and cortex, as well as for experience-dependent alterations in systems-level hippocampal connectivity. We focus on reactivation during awake post-encoding periods, relationships between reactivation and subsequent behavior, how reactivation is modulated by factors that influence consolidation, and the implications of persistent reactivation for biasing ongoing perception and cognition

Fear not: recent advances in understanding the neural basis of fear memories and implications for treatment development.

Fear is a highly adaptive emotion that has evolved to promote survival and reproductive fitness. However, maladaptive expression of fear can lead to debilitating stressor-related and anxiety disorders such as post-traumatic stress disorder. Although the neural basis of fear has been extensively researched for several decades, recent technological advances in pharmacogenetics and optogenetics have allowed greater resolution in understanding the neural circuits that underlie fear. Alongside conceptual advances in the understanding of fear memory, this increased knowledge has clarified mechanisms for some currently available therapies for post-traumatic stress disorder and has identified new potential treatment targets

The Modulatory Influences of Amygdala-Hippocampal Interactions on Emotional Memory

This thesis is a literature review on the effects that emotion has on memory. The influences that emotion has on memory will be analyzed, specifically through the lens of amygdala-hippocampal interactions. Primary focus will be on the compilation and analysis of emotional memory studies, and how the enhancement of emotional memories is facilitated by amygdala-hippocampal modulation. By viewing brain activity and the direct or indirect projections to and from these specific brain regions, I will provide a cohesive, critical literature review of relevant cognitive neuroscience work on emotional memory and amygdala-hippocampus connections. By compiling relevant cognitive neuroscience findings in one thesis, this will make it easier to understand and comprehend the amygdala-hippocampal interconnection and its impact on emotional memory

It's the intention that matters : neural representations of learning from intentional harm in social interactions

As a social species, humans are not only driven by the pursuit of necessities such as food and shelter, but also complex processes such as social interactions. To navigate our everyday life, we use information gathered throughout a lifetime of social interactions in which we learn from others and their actions but also, and not less importantly, about others. To create a complete picture of a social interaction, we assess the individual we interact with, make judgements about them and their actions, and integrate what we know with the consequences of their actions. This way, we learn the relationship between events (e.g. others’ actions) and environmental stimuli, such as other individuals that predict the actions. As we encounter more people and go through more interactions, we continuously update information stored in memory from previous experiences. A common task, for example, going through the busy corridor in our workplace in a hurry does not only include avoiding physical harm caused by bumping into the coffee machine with a sharp corner, but also avoiding a co-worker we are in a feud with, and whom we believed knowingly spilled hot coffee on another co-worker the week before. How social information is processed is key in understanding rarer but more impactful events that can have lifelong impact on an individual’s life. Interpersonal trauma, a type of trauma that is acquired from harm received from another individual, leads more often to post-traumatic stress disorder (PTSD) than non-socially related trauma, for example, a car crash (Kleim, Ehlers, & Glucksman, 2007). To understand why a specific social harm affect us negatively, it is crucial to study how the brain integrates social, as well as nonsocial (physical) information during the harmful event. In Study I, II, and III we investigated how different streams of information (social and physical) are integrated during a social interaction. We were interested in how intentionality of an action that has direct aversive consequences on an individual can change the individuals’ judgements of the action and the person performing it. Using a time-based neuroimaging approach, we investigated how the value of an action is integrated with that of the intention behind it. Study I revealed evidence that suggests that intentionality of a directly experienced aversive action is represented throughout the cortex in neural activity patterns that form over time. Study II highlighted the importance of timing and sample size in similar paradigms, and that neural pattern formation in response to aversive actions regardless of the intentions behind them are robustly replicated. In Study III we asked questions about how these learned action outcomes and knowledge about the people performing the harmful action change neural connectivity, and how this translates into changes in perception and memory 24-hours later. We found an increased connectivity between the hippocampus and the amygdala, which correlated with generalized memory responses to images associated with shocks from an intentional harm do-er, and increased connectivity between the FFA and the insula, as well as the FFA and the dorsomedial prefrontal cortex (dmPFC) correlated with facilitated recognition of the intentional harm do-er’s face

Valence-specific Enhancements in Visual Processing Regions Support Negative Memories:

Thesis advisor: Elizabeth A. KensingerResearch in four parts examines the effects of valence on the neural processes that support emotional memory formation and retrieval. Results show a consistent valence-specific enhancement of visuocortical engagement along the ventral visual stream and occipital cortex that supports negative memories to a greater extent than positive memories. Part I investigated the effects of valence on the interactions between trial-level physiological responses to emotional stimuli (i.e., heart rate deceleration) during encoding and subsequent memory vividness. Results showed that negative memory vividness, but not positive or neutral memory vividness, is tied to arousal-related enhancements of amygdala coupling with early visual cortex during encoding. These results suggest that co-occurring parasympathetic arousal responses and amygdala connectivity with early visual cortex during encoding influence subsequent memory vividness for negative stimuli, perhaps reflecting enhanced memory-relevant perceptual enhancements during encoding of negative stimuli. Part II examined links between individual differences in post-encoding increases is amygdala functional connectivity at rest and the degree and direction of emotional memory biases at retrieval. Results demonstrated that post-encoding increases in amygdala resting state functional connectivity with visuocortical and frontal regions predicted the degree of negative memory bias (i.e., better memory for unpleasant compared to pleasant stimuli) and positive memory bias, respectively. Further, the effect of amygdala-visuocortical post-encoding coupling on behavioral negative memory bias was completely mediated by greater retrieval-related activity for negative stimuli in visuocortical areas. These findings suggest that those individuals with a negative memory bias tend to engage visual processing regions across multiple phases of memory more than individuals with a positive memory bias. While Parts I-II examined encoding-related memory processes, Part III examined the effects of valence on true and false subjective memory vividness at the time of retrieval. The findings showed valence-specific enhancements in regions of the ventral visual stream (e.g., inferior temporal gyrus and parahippocampal cortex) support negative memory vividness to a greater extent than positive memory vividness. However, activation of the parahippocampal cortex also drove a false sense of negative memory vividness. Together, these findings suggest spatial overlap in regions that support negative true and false memory vividness. Lastly, Part IV utilized inhibitory repetitive transcranial magnetic stimulation (rTMS) to test if a portion of occipito-temporal cortex that showed consistent valence-specific effects of negative memory in Parts I-III was necessary for negative memory retrieval. Although some participants showed the hypothesized effect, there was no group-level evidence of a neuromodulatory effect of occipito-temporal cortex rTMS on negative memory retrieval. Together, the results of the current dissertation work highlight the importance of valence-based models of emotional memory and consistently implicated enhanced visuosensory engagement across multiple phases of memory. By identifying valence-specific effects of trial-level physiological arousal during encoding, post-encoding amygdala coupling during early consolidation, and similarities and differences between true and false negative memories, the present set of work has important implications for how negative and positive memories are created and remembered differently.Thesis (PhD) — Boston College, 2019.Submitted to: Boston College. Graduate School of Arts and Sciences.Discipline: Psychology