A mixed methods experience sampling study of a posttraumatic growth model for addiction recovery.

Problematic substance use and addiction is a growing crisis in the United States. As a result, identifying factors that effectively promote addiction recovery is, currently, of particular societal importance. Informed by evidence that-while addiction can be perpetuated by stress-related impulsivity and decreased self-regulation-perceived social support is protective against addiction, we test a model for addiction recovery as a form of posttraumatic growth (PTG), focused specifically on close relationships and personal strength-two domains of PTG. In an initial study, we found that perceived social support and impulsivity predicted number of relapses in individuals in a substance use disorder recovery program. Using experience sampling, we then observed that experiencing a stressful event predicted impulsive behavior. However, experiencing closeness with others-a domain of PTG-was directly associated with perceived social support, and both predicted positive emotional states, which were, in turn, inversely associated with experiencing a stressful event. Further, when experiencing a stressful event, personal strength-also a domain of PTG-was inversely associated with impulsive behavior and was predicted by both perceived social support and positive emotional states. Finally, in a follow-up experiment, we found that an ecological momentary intervention targeting perceived social support decreased impulsivity and increased self-regulation-an aspect of personal strength-in a dose-dependent fashion. Taken together, our findings: (1) support a PTG model for recovery; (2) provide evidence for processes by which close supportive relationships are protective against addiction and relapse; and (3) indicate that self-regulation is responsive to a short in-the-moment perceived social support intervention. We suggest that these findings support the theory that addiction is a social disease in the sense that close personal interactions and supportive relationships: (a) buffer against stress-related impulsivity, thereby protecting against addiction and relapse; and (b) increase personal strength, thereby decreasing the probability of impulsive-including addictive-behavior and promoting recovery.

Evidence for the standard model, multiple trace theory, or the unified theory?

There have been two dominating theories for memory consolidation: the standard model (SM) and multiple trace theory (MTT). Whereas lesion studies have largely indicated a waning role for the hippocampus in memory consolidation, and thus have supported SM, findings from neuroimaging studies have produced varying results. Tallman et al. (this issue) argue that this variability may result from confounding factors and that, once these factors are accounted for, their neuroimaging results support SM. They do not, however, consider a third option: the unified theory. Here, we suggest that their findings, along with neurobiochemical and engram cell studies, may better fit this third theory.

Coordinating what we've learned about memory consolidation: Revisiting a unified theory.

According to traditional systems consolidation theories neocortical long-term plasticity (i.e., cellular consolidation) lags behind, and is dependent upon, hippocampal long-term plasticity. In this review, we examine accumulating evidence that local neocortical and hippocampal cellular consolidation occurs with a similar time-course. The implication is that the rate-limiting step for systems consolidation is the time it takes for cellular consolidation in longer connections throughout a more distributed extra-hippocampal system that comes to coordinate distributed neocortical activity during recall. The hippocampus is, thus, crucial for the development of this extra-hippocampal coordinating system, and acts to coordinate activities crucial for recall until it develops. Recent work on schema formation, engram cells, and the role of sleep in consolidation add substantial evidence for this "unified theory" of systems and cellular consolidation. Here, we discuss this evidence, its implications, and consider remaining questions.

Using experience sampling to examine links between compassion, eudaimonia, and pro-social behavior.

OBJECTIVE: Compassion has been associated with eudaimonia and pro-social behavior, and it has been regarded as a virtue, both historically and cross-culturally. However, the psychological study of compassion has been limited to laboratory settings and/or standard survey assessments. Here, we use an experience sampling method (ESM) to compare naturalistic assessments of compassion with standard assessments, and to examine compassion, its variability, and associations with eudaimonia and pro-social behavior. METHOD: Undergraduate students (n = 200) took a survey that included standard assessments of compassion and eudaimonia. Then, over 4 days, they were repeatedly asked about their level of compassion, eudaimonia, and situational factors within the moments of daily life. Finally, pro-social behavior was tested using the Dual Gamble Task and an opportunity to donate task winnings. RESULTS: Analyses revealed within-person associations between ESM compassion and eudaimonia. ESM compassion also predicted eudaimonia at the next ESM time point. While not impervious to situational factors, considerable consistency was observed in ESM compassion in comparison with eudaimonia. Further, ESM compassion along with eudaimonia predicted donating behavior. Standard assessments did not. CONCLUSIONS: Consistent with virtue theory, some individuals' reports were indicative of a probabilistic tendency toward compassion, and ESM compassion predicted ESM eudaimonia and pro-social behavior toward those in need.

Smartphone delivery of a hope intervention: Another way to flourish.

Positive interventions have shown promise for fostering hedonic (happiness) and eudaimonic (flourishing) well-being. However, few studies have focused on positive interventions that target hope as a means of increasing well-being, and none have examined the use of smartphone app-based systems for delivering interventions in the moments and contexts of daily life-an approach called ecological momentary intervention (EMI). We conducted a quasi-experimental pilot study using a pretest and posttest design to examine the feasibility and potential impact of a mobile app-based hope EMI. Participants appeared to engage with the intervention and found the experience to be user-friendly, helpful, and enjoyable. Relative to the control group, those receiving the intervention demonstrated significantly greater increases in hope; however, there were no between-group differences in hedonic and eudaimonic well-being. The authors recommend future research to examine the potential of EMI mobile apps to cultivate hope and promote flourishing.

Virtues, ecological momentary assessment/intervention and smartphone technology.

Virtues, broadly understood as stable and robust dispositions for certain responses across morally relevant situations, have been a growing topic of interest in psychology. A central topic of discussion has been whether studies showing that situations can strongly influence our responses provide evidence against the existence of virtues (as a kind of stable and robust disposition). In this review, we examine reasons for thinking that the prevailing methods for examining situational influences are limited in their ability to test dispositional stability and robustness; or, then, whether virtues exist. We make the case that these limitations can be addressed by aggregating repeated, cross-situational assessments of environmental, psychological and physiological variables within everyday life-a form of assessment often called ecological momentary assessment (EMA, or experience sampling). We, then, examine how advances in smartphone application (app) technology, and their mass adoption, make these mobile devices an unprecedented vehicle for EMA and, thus, the psychological study of virtue. We, additionally, examine how smartphones might be used for virtue development by promoting changes in thought and behavior within daily life; a technique often called ecological momentary intervention (EMI). While EMA/I have become widely employed since the 1980s for the purposes of understanding and promoting change amongst clinical populations, few EMA/I studies have been devoted to understanding or promoting virtues within non-clinical populations. Further, most EMA/I studies have relied on journaling, PDAs, phone calls and/or text messaging systems. We explore how smartphone app technology provides a means of making EMA a more robust psychological method, EMI a more robust way of promoting positive change, and, as a result, opens up new possibilities for studying and promoting virtues.

A smartphone ecological momentary assessment/intervention "app" for collecting real-time data and promoting self-awareness.

We have designed a flexible ecological momentary assessment/intervention smartphone (EMA/EMI) "app". We examine the utility of this app for collecting real-time data, and assessing intra-subject variability, by using it to assess how freshman undergraduates spend their time. We also explore whether its use can promote greater self-awareness. Participants were randomly divided into an experimental group, who used the app, and a control group, who did not. We used the app to collect both randomized in-the-moment data as well as end-of-day data to assess time use. Using a posttest survey we asked participants questions about how they spent time throughout the school semester. We also asked the experimental group about their experience with the app. Among other findings, 80.49% participants indicated that they became more aware of how they spent their time using the app. Corroborating this report, among the experimental group, end-of-semester self-assessment of time spent wasted, and time spent using electronics recreationally, predicted semester GPA at a strength comparable to high school GPA and ACT score (two of the best single predictors for first semester college GPA), but had no correlation among controls. We discuss the advantages and limitations of using apps, such as ours, for EMA and/or EMI.

Neuroscience exposure and perceptions of client responsibility among addictions counselors.

Members of the National Association of Alcoholism and Drug Abuse Counselors (n = 231) participated in a survey concerning their view of the role of personal responsibility in addictions treatment and its relation to their exposure to neuroscience (i.e., the amount to which members considered themselves familiar with current neuroscience research). We used the two-dimensional model of responsibility (Responsible/not responsible for development × Responsible/not responsible for recovery) proposed by P. Brickman et al. (1982) to guide our assessment of responsibility, thus inquiring about counselors' views of clients' responsibility for both the development of a substance-related addiction and its resolution. Findings suggest that counselors rate biological factors as most influential in the development of an addiction and assign clients less personal responsibility for the development of an addiction than for recovery from an addiction. Counselors' level of neuroscience exposure was negatively correlated with their ratings of client responsibility for the development of an addiction but positively correlated to ratings of client responsibility for recovery. This suggests that counselors are integrating neuroscientific findings with what is learned from other modes of enquiry in a way that diminishes the view that clients are responsible for addiction development but accentuates the view that clients are responsible for recovery. We explore reasons for why this is and why this approach may be beneficial.

Molecular activity underlying working memory.

The prefrontal cortex is necessary for directing thought and planning action. Working memory, the active, transient maintenance of information in mind for subsequent monitoring and manipulation, lies at the core of many simple, as well as high-level, cognitive functions. Working memory has been shown to be compromised in a number of neurological and psychiatric conditions and may contribute to the behavioral and cognitive deficits associated with these disorders. It has been theorized that working memory depends upon reverberating circuits within the prefrontal cortex and other cortical areas. However, recent work indicates that intracellular signals and protein dephosphorylation are critical for working memory. The present article will review recent research into the involvement of the modulatory neurotransmitters and their receptors in working memory. The intracellular signaling pathways activated by these receptors and evidence that indicates a role for G(q)-initiated PI-PLC and calcium-dependent protein phosphatase calcineurin activity in working memory will be discussed. Additionally, the negative influence of calcium- and cAMP-dependent protein kinase (i.e., calcium/calmodulin-dependent protein kinase II (CaMKII), calcium/diacylglycerol-activated protein kinase C (PKC), and cAMP-dependent protein kinase A (PKA)) activities on working memory will be reviewed. The implications of these experimental findings on the observed inverted-U relationship between D(1) receptor stimulation and working memory, as well as age-associated working memory dysfunction, will be presented. Finally, we will discuss considerations for the development of clinical treatments for working memory disorders.

Inhibition of prefrontal protein synthesis following recall does not disrupt memory for trace fear conditioning.

BACKGROUND: The extent of similarity between consolidation and reconsolidation is not yet fully understood. One of the differences noted is that not every brain region involved in consolidation exhibits reconsolidation. In trace fear conditioning, the hippocampus and the medial prefrontal cortex (mPFC) are required for consolidation of long-term memory. We have previously demonstrated that trace fear memory is susceptible to infusion of the protein synthesis inhibitor anisomycin into the hippocampus following recall. In the present study, we examine whether protein synthesis inhibition in the mPFC following recall similarly results in the observation of reconsolidation of trace fear memory. RESULTS: Targeted intra-mPFC infusions of anisomycin or vehicle were performed immediately following recall of trace fear memory at 24 hours, or at 30 days, following training in a one-day or a two-day protocol. The present study demonstrates three key findings: 1) trace fear memory does not undergo protein synthesis dependent reconsolidation in the PFC, regardless of the intensity of the training, and 2) regardless of whether the memory is recent or remote, and 3) intra-mPFC inhibition of protein synthesis immediately following training impaired remote (30 days) memory. CONCLUSION: These results suggest that not all structures that participate in memory storage are involved in reconsolidation. Alternatively, certain types of memory-related information may reconsolidate, while other components of memory may not.

Distinct prefrontal molecular mechanisms for information storage lasting seconds versus minutes.

The prefrontal cortex (PFC) is known to actively hold information "online" for a period of seconds in working memory for guiding goal-directed behavior. It has been proposed that relevant information is stored in other brain regions, which is retrieved and held in working memory for subsequent assimilation by the PFC in order to guide behavior. It is uncertain whether PFC stores information outside the temporal limits of working memory. Here, we demonstrate that although enhanced cAMP-dependent protein kinase A (PKA) activity in the PFC is detrimental to working memory, it is required for performance in tasks involving conflicting representations when memory storage is needed for minutes. This study indicates that distinct molecular mechanisms within the PFC underlie information storage for seconds (working memory) and for minutes (short-term memory). In addition, our results demonstrate that short-term memory storage within the prefrontal cortex is required for guiding behavior in tasks with conflicts and provides a plausible mechanism by which the prefrontal cortex executes cognitive control.

A role for prefrontal calcium-sensitive protein phosphatase and kinase activities in working memory.

The prefrontal cortex is involved in the integration and interpretation of information for directing thoughts and planning action. Working memory is defined as the active maintenance of information in mind and is thought to lie at the core of many prefrontal functions. Although dopamine and other neurotransmitters have been implicated, the intracellular events activated by their receptors that influence working memory are poorly understood. We demonstrate that working memory involves transient changes in prefrontal G(q/11)-signaling and in calcium-dependent intracellular protein phosphatase and kinase activity. Interestingly, inhibition of the calcium activated phosphatase calcineurin impaired, while calcium/calmodulin dependent kinase II (CaMKII) and calcium-dependent protein kinase C (PKC) enhanced, working memory. Our findings suggest that the active maintenance of information required for working memory involves transient changes in the balance of these enzymes' activities.

Inhibition of hippocampal protein synthesis following recall disrupts expression of episodic-like memory in trace conditioning.

Transition of short-term to long-term memory is referred to as consolidation and the process is dependent on protein synthesis. Recently, several studies have shown that expression of consolidated memory for simple forms of learning tasks (e.g., delay conditioning, contextual fear, inhibitory avoidance) becomes vulnerable to disruption by inhibition of protein synthesis when administered shortly after recall. In the present study, we address whether recall-induced dependence on protein synthesis is a fundamental property that can be applied to a form of memory requiring attentional awareness or is specific to memories for simple forms of conditioning. Trace fear conditioning is a form of learning that requires an active memory trace to associate a conditioned stimulus (CS) with an unconditioned stimulus (US) separated by time. Our data demonstrate that whether a CS-alone recall trial in a novel context acts as an extinction or reactivation trial depends on the strength of the original memory. Inhibition of protein synthesis following the recall trial in animals receiving one trace conditioning training session (that gives rise to weak memory) resulted in enhanced CS-elicited freezing compared with vehicle control, as a result of impaired extinction memory, but had no effect on contextual memory. However, inhibition of hippocampal protein synthesis following the recall trial in animals receiving two trace conditioning training sessions (that gives rise to stronger memory) resulted in impaired retention of both trace CS-US associative and contextual memory despite that the context-US association was not directly reactivated. This provides evidence that, for a robust memory, the CS-alone recall trial results in the reactivation of an episodic-like memory, including trace CS- and contextual-memory, and that hippocampal information storage for the memory as a whole is returned to a labile state requiring de novo protein synthesis. This and other studies are consistent with the role of the hippocampus in coordinating episodic memory retrieval.

Intra-medial prefrontal administration of SCH-23390 attenuates ERK phosphorylation and long-term memory for trace fear conditioning in rats.

The prefrontal cortex is known to be involved in the acquisition of trace conditioning, a higher-cognitive form of Pavlovian conditioning in which a conditioned stimulus and an unconditioned stimulus are separated by a time gap. We have recently reported that medial prefrontal (mPFC) extracellular-signal regulated kinase (Erk) phosphorylation is involved in the long-term memory storage of trace fear conditioning. Because of the important role dopamine D1 receptors play in prefrontal function, such as working memory, and due to evidence that dopamine D1 receptor activity can modulate plasticity, we investigated their role in prefrontal Erk phosphorylation following trace fear conditioning. We found that inhibition of dopamine D1 receptors through intra-mPFC infusion of SCH-23390 (1 microg/0.5 microL) 15 min prior to trace fear conditioning resulted in a decrease in training-related Erk phosphorylation. Additionally, pre-training intra-mPFC infusion of SCH-23390 also resulted in the impairment of long-term retention of CS-US association. These findings implicate mPFC dopamine D1 receptor activity in the storage of long-term memory for higher-cognitive associative tasks.

A unified theory for systems and cellular memory consolidation.

The time-limited role of the hippocampus for explicit memory storage has been referred to as systems consolidation where learning-related changes occur first in the hippocampus followed by the gradual development of a more distributed memory trace in the neocortex. Recent experiments are beginning to show that learning induces plasticity-related molecular changes in the neocortex as well as in the hippocampus and with a similar time course. Present memory consolidation theories do not account for these findings. In this report, we present a theory (the C theory) that incorporates these new findings, provides an explanation for the length of time for hippocampal dependency, and that can account for the apparent longer consolidation periods in species with larger brains. This theory proposes that a process of cellular consolidation occurs in the hippocampus and in areas of the neocortex during and shortly after learning resulting in long-term memory storage in both areas. For a limited time, the hippocampus is necessary for memory retrieval, a process involving the coordinated reactivation of these areas. This reactivation is later mediated by longer extrahippocampal connectivity between areas. The delay in hippocampal-independent memory retrieval is the time it takes for gene products in these longer extrahippocampal projections to be transported from the soma to tagged synapses by slow axonal transport. This cellular transport event defines the period of hippocampal dependency and, thus, the duration of memory consolidation. The theoretical description for memory consolidation presented in this review provides alternative explanations for several experimental observations and presents a unification of the concepts of systems and cellular memory consolidation.

A role for prefrontal cortex in memory storage for trace fear conditioning.

The prefrontal cortex has been shown to participate in the association of events separated by time. However, it is not known whether the prefrontal cortex stores the memory for these relationships. Trace conditioning is a form of classical conditioning in which a time gap separates the conditioned stimulus (CS) from the unconditioned stimulus (US), the association of which has been shown to depend on prefrontal activity. Here we demonstrate that inhibition of extracellular signal-regulated kinase (Erk) cascade (a biochemical pathway involved in long-term memory storage) in the rat medial prefrontal cortex did not interfere with memory encoding for trace fear conditioning but impaired memory retention. In addition, animals displayed impaired memory for the irrelevancy of the training context. Hippocampal Erk phosphorylation was found to have a later time course than prefrontal Erk phosphorylation after trace fear conditioning, indicating a direct role for the prefrontal cortex in associative memory storage for temporally separated events as well as in memory storage of relevancy.