Emotional enhancement of memory: how norepinephrine enables synaptic plasticity

Changes in synaptic strength are believed to underlie learning and memory. We explore the idea that norepinephrine is an essential modulator of memory through its ability to regulate synaptic mechanisms. Emotional arousal leads to activation of the locus coeruleus with the subsequent release of norepineprine in the brain, resulting in the enhancement of memory. Norepinephrine activates both pre- and post-synaptic adrenergic receptors at central synapses with different functional outcomes, depending on the expression pattern of these receptors in specific neural circuitries underlying distinct behavioral processes. We review the evidence for noradrenergic modulation of synaptic plasticity with consideration of how this may contribute to the mechanisms of learning and memory

An investigation of propranolol as an agent for the experimental manipulation of interoception.

Interoception has recently come under research focus as a potential influence on emotional and epistemic feelings. However, existing means to manipulate it experimentally have conceptual or logistical drawbacks. We investigated whether 20 mg of propranolol is a viable agent for experimentally manipulating interoception. Thirteen participants completed a double-blind, placebo-controlled crossover study, performing two heartbeat perception tasks, control tasks and measures of anxiety and alertness. All measures were obtained at the beginning and end of both sessions. Propranolol significantly decreased heart rate and systolic blood pressure. Heartbeat detection performance numerically decreased under propranolol, although this effect failed to reach statistical significance. Heartbeat tracking exhibited a practice effect in both sessions. There were no significant effects on the control tasks. State anxiety was unchanged within either session, and alertness decreased in both. These findings validate the propranolol paradigm, and the numerical change in heartbeat detection warrants follow-up with a larger sample

The False Hope of Deliberate Forgetting: A Critical Response to Proponents of Limited-Use Memory Manipulation

The emergence of manipulation techniques that dampen, disassociate, erase, and replace unsavory episodic memories have given pause to even the most ardent proponents of the practice. Supporters of memory manipulation have since clarified that the interventions should be made available exclusively in extreme and limited-use cases. In light of the narrowing of this approach, the present essay examines the arguments in favor of limited-use memory manipulation (LUMM) for the two most commonly-cited circumstances in which the practice is claimed to be justified: post-traumatic stress disorder (PTSD) and substance addiction. After examining the neuroscience of PTSD and substance addition, the critical concepts of biomedicalization and the codification of new diseases, the myth of global autonomy loss, and the terminal normlessness of LUMM are explored to underscore the false hope of deliberate forgetting

Acute effects of alcohol on trauma memories

Memory disturbances following a trauma are a characteristic feature of posttraumatic stress disorder. Despite alcohol’s frequent involvement in real-life traumatic events, our understanding of its contribution to trauma-related symptoms is unclear. The research in this thesis aimed to determine the way in which alcohol intoxication during a traumatic experience might influence memory for the event. Experiment 1 showed that alcohol impaired recognition associated with recollection with greater reductions as dose increased (0, 0.4, 0.6, 0.8g/kg); in contrast, recognition associated with familiarity was preserved. Experiments 2 and 3 utilised an analogue trauma film to examine how low (0.4g\kg) and high (0.8g/kg) doses of alcohol affected intrusive imagery and explicit memory for the footage. Alcohol during encoding resulted in a dose-dependent inverted U-shaped curve on intrusive imagery, with increased intrusions only following a low dose. Explicit memory for the footage was reduced in a dose-dependent linear manner. In addition, experiment 3 concurrently assessed same- and shifted-view object location recognition to determine the mechanisms that might underpin alcohol’s effects on trauma memory. Results showed that a low dose of alcohol selectively impaired shifted-view recognition, thought to rely on an allocentric representation. However, same-view recognition was preserved, suggesting a spared egocentric representational system. In contrast, the high dose disrupted both same- and shifted-view recognition, suggesting a global disruption in both memory systems. Experiment 4 examined the effects of alcohol (0.4/kg) on contextual fear acquisition and extinction and both same- and shifted-view recognition. Fear acquisition was unaffected by alcohol, whilst extinction learning was impaired with persistent conditioned responses throughout extinction. Alcohol-induced reductions in extinction learning were highly correlated with decreases in shifted-view recognition, supporting the role of contextual encoding in extinction. The findings of these studies suggest that alcohol dose-dependently influences trauma memories and this could result in a distinct set of trauma-related symptoms

Testing the Network Reset Hypothesis: Noradrenergic Modulation of Hippocampal Representations

The locus coeruleus (LC) responds to salience cues, including novelty, and sends a major noradrenergic projection to the hippocampal formation (HF). Novelty-associated LC activation may help to sculpt contextual representations in the HF, but modulatory influence of norepinephrine (NE) over HF representations remains poorly understood. One possible mechanism is that NE provides a “reset” signal causing the HF to recruit distinct neural populations, thereby providing a molecular switch to dictate if hippocampal circuits should generate new representations or update existing ones to incorporate novel information. This hypothesis suggests that NE release should cause the HF to recruit a unique population even in the presence of the same stimuli an animal has just experienced, a phenomenon referred to as “global remapping”. The compartmental expression of immediate early genes (i.e. arc & zif268) allowed us to test this by mapping the activity history of individual neurons as animals engaged in spatial processing following LC-NE manipulation. Recruitment of new neurons is part of the memory encoding process involved in separating memories. Tasks involving memory retrieval require reactivation of representations formed during encoding. If those representations “remapped” (i.e. a new cellular ensemble was recruited, rather than reactivation of the cells comprising the previously formed representation), this should theoretically result in a retrieval error. Therefore, switching the system back to a state of encoding would prove maladaptive in situations where retrieval is necessary to perform a task, unless new information was at hand. We hypothesize that NE resets the system causing the HF to move from a state of retrieval back to encoding when it is necessary, when novel information needs to be incorporated. This hypothesis suggests the effect of modulating NE on memory critically depends on the stage of training. To further understand how NE modulation of hippocampal circuits affects spatial memory, we tested whether infusions of the β-adrenergic agonist isoproterenol would impair working and reference memory retrieval (i.e., switching the system back to encoding when it is maladaptive) and in contrast, promote cognitive flexibility thus improving reversal learning (i.e., switching the system back to encoding when it is adaptive)

Memory for Emotional Images: Mechanisms of Episodic Processing and its Psychophysiological Correlates

Negative emotional stimuli are usually better remembered than neutral emotional stimuli. Previous examination of binding theory found no differences in recall for pure lists of taboo and neutral words. A similar result was found with equivalent recognition memory performance between pure lists of negative, positive, and neutral images. The current research is designed to test the predictions of binding theory using negative and neutral visual stimuli in mixed lists. A rapid serial visual presentation paradigm and recognition memory item-discrimination tasks are used. Binding theory predicts differences in recognition memory performance between arousing and neutral images in mixed lists, but not pure lists. Skin conductance and heart rate data are collected to understand the physiological counterparts of the psychological processes in episodic memory. Results found equivalent recognition memory performance between negative and neutral images in mixed and pure lists. A significant liberal response bias for negative over neutral images was observed across experiments. Skin conductance and heart rate measures did not correlate with recognition memory performance