University of Groningen
Motivation, reward and stress: individual difference and neural basis
Xin, Yuanyuan
DOI:
10.33612/diss.143843592
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Xin, Y. (2020). Motivation, reward and stress: individual difference and neural basis. University of Groningen. https://doi.org/10.33612/diss.143843592
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CHAPTER 6
General Discussion
1 Summary of findings
Chapter 2 revealed that higher neuroticism predicted lower cardiovascular response, lower HPA axis response, a stronger decline of positive affect and a weaker control-feeling during the Trier Social Stress Test (TSST). Higher extraversion was associated with less cortisol activation and a slower increase in negative affect during the TSST. Higher scores on openness were – like higher extraversion –also associated with a lower cortisol stress response. These results showed that the different personality traits were associated with differences in several aspects of individual stress responses.
In Chapter 3, we found that the number of life event exposure during the past 12 months was associated with a blunted heart rate and a lower heart rate variability (HRV) reactivity to the TSST after controlling for individual differences in neuroticism. Furthermore, the group with low executive control (higher false alarm rate in the Go/No-Go task) showed a significant association between higher recent life stress and blunted acute stress response, which was not apparent in the group with high executive control (lower false alarm rate in the Go/No-Go task). These results suggested that greater executive control may benefit us with adaptive acute stress responses under recent life stress. Chapter 4 integrated fMRI studies in a meta-analysis of reward processing under acute stress, showing that acute stress enhanced reward anticipation, the motivation/incentive component of reward, in the bilateral putamen,
whereas reward consumption, the pleasure of getting a reward, was decreased under acute stress in the dorsal striatum and right thalamus. These findings have important implications for understanding real-world reward-related behavior in stressful environments.
Chapter 5 examined the relationship between trait motivation and time-money tradeoff choices. It showed that individuals with higher trait motivation had a greater propensity to choose an immediate small reward over a more ‘rational but delayed’ reward, which was modulated by the functional coupling of the dorsolateral prefrontal cortex (dlPFC) with the medial prefrontal cortex (mPFC). These results suggested that intrinsic organization within the
prefrontal cortex plays a key role in linking achievement motivation and reward discounting behavior.
In the following, I will discuss potentially unifying neurobiological and psychological mechanisms that may underlie individual differences in acute stress responses and the interaction between stress and reward processing.
2 Possible mechanisms underlying individual differences in
acute stress responses
Chapter 2 revealed that neuroticism was the strongest predictor of blunted cortisol response to TSST among the five personality factors. Neuroticism is a general risk factor associated with many forms of psychopathology, such as anxiety and depression (Kotov et al. 2010) which were also found associated with an altered HPA response to acute stress (Fiksdal et al. 2019; Zorn et al. 2017). However, the underlying mechanisms have not been fully elucidated yet. Based on previous studies, I discuss plausible psychological and neural
mechanisms for altered acute stress responses from three angles: emotion processing and amygdala, cognitive control and prefrontal cortex, and the reward-motivation dopamine system (see also Figure 1).
2.1 Altered emotion processing and amygdala function
Personality refers to a stable pattern of behavior and emotional responses. The particular way a person perceives a situation determines how he or she would cope with it behaviorally and physiologically (McEwen 1998). Altered emotion processing is one of the core symptoms in a number of personality disorders and has been associated with increased rates of transdiagnostic psychopathology. For instance, greater emotion responses pre-exposure to stressful military service were associated with increased levels of stress disorder symptoms post-exposure (Admon et al. 2013). Neuroticism is
generally characterized by altered emotion processing (for a review, Servaas et al. 2013). For example, it is associated with self-reported difficulties regulating emotions (Paulus et al. 2016) as well as with problematic coping strategies such as wishful thinking, withdrawal, and emotion-focused coping (Connor-Smith and Flachsbart 2007; Ormel et al. 2013). Evidence from brain imaging studies corroborate these findings. One electroencephalography (EEG) study reported that neurotic individuals appraise unknown information as more negative, as indexed by a greater feedback related negativity (ERN) to uncertainty than to positive stimuli (Hirsh and Inzlicht 2008). A systematic review with fMRI studies showed that activity in the amygdala, a key hub for emotion processing in the brain (for a review, Phelps and LeDoux 2005), was associated with higher cortisol responses both during and shortly after acute stress (Harrewijn et al. 2020). Moreover, high-neurotic individuals showed
enhanced amygdala reactivity to acute stress (Everaerd et al. 2015).
Given the evidence of altered emotion processing and increased amygdala reactivity to aversive stimuli in high neurotic individuals, the blunted
cardiovascular and cortisol stress response in high neuroticism as we observed in Chapter 2 may be a reflection of vulnerability to the development of affective disorders. However, it should be noted that neuroticism is a multi-faceted, complex construct comprising anxiety, depression, self-consciousness, impulsivity and hostility (Weiss and Costa 2005). Thus, further studies are needed to know which specific dimensions of neuroticism play a key role in stress vulnerability.
2.2 Altered cognitive control and frontal cortex
Cognitive control has been proposed to underlie the ability of emotion regulation (Ochsner et al. 2012; Joormann and Tanovic 2015). Revealing the complexity of this relationship, all aspects of cognitive control, including updating (constant monitoring and rapid addition/deletion of working memory contents), shifting (switching flexibly between tasks or mental sets) and inhibition (deliberate overriding of dominant or prepotent responses) (Miyake and Friedman 2012), are associated with different components of emotion processing. For example, updating ability was found to moderate the effect of reappraisal and rumination on negative stimuli (Joormann and Tanovic 2015), indicating that cognitive control influences stress responses indirectly. This was supported by the study in Chapter 3, where we found a moderating role of cognitive control in the relationship between life event frequency in the last 12 months and cardiovascular response to TSST. Specifically, the association between higher exposure to life events and blunted acute stress response was not apparent in the high inhibitory control group. As one dimension of cognitive control, inhibition was considered as the capacity to override an initially
dominant response, whereas inhibition deficiency is associated with impairment in disengaging from negative emotions (Joormann and Tanovic 2015).
Alterations in cognitive control of emotion were also observed in individuals of high neuroticism. Specifically, trait neuroticism was associated with decreased function connectivity between anterior cingulate cortex (ACC) and amygdala (Cremers et al. 2010) and with a failure in top-down control and regulation of emotion in the neurocircuitry of amygdala-ventromedial prefrontal cortex (VMPFC) connectivity (Silverman et al. 2019). Further, neuroticism was related to increased activation in brain regions of frontal and cingulate areas involved in
the processing and regulation of emotion, possibly suggesting a need for greater regulatory efforts in order to gain cognitive control over negative emotions (for a review, Servaas et al. 2013). In addition, HRV was recently proposed as a biomarker of top-down self-regulation of behavioral, cognitive, and emotional processes (for a review, Holzman and Bridgett 2017), but reduced high-frequency HRV during cognitive reappraisal of negative stimuli was observed in high neuroticism (Di Simplicio et al. 2012). Though the specific-focused study on the cognitive control and acute stress response is still scarce, this evidence suggests that greater executive control may be beneficial in terms of a more adaptive response to acute stress. Investigating cognitive control in different groups with different stress responses in future research will provide important insights into the potential determinants which make a person able to cope with, recover from, and develop resilience to stress.
2.3 Altered motivation-reward processing and dopamine activity
In addition to the well-known stress hormone cortisol, we also described how dopamine reacts to acute stress dynamically in the Introduction section. Dopamine is typically considered the core modulator of the reward-motivation system in both monkeys and humans (Schultz 2015). Recently, an alternative fresh perspective was raised that dopamine plays a general role in dynamically estimating of whether or not to expend a limited internal resource, such as energy, attention, or time (Berke 2018; Westbrook et al. 2020). Taken together, the dopamine system may be as important as the HPA axis in
individual responses to acute stress. Specifically, cortisol seems to prepare the body for a response to acute stress, whereas the dopamine response may be a compensative preparation of the mind in terms of a decision process of how to cope with a given stress situation. Though the exact relationship between dopamine and cortisol in one’s response to acute stress is not fully understood in humans, there is evidence that the two systems dynamically interact with one another. One study observed a positive association between cortisol levels to psychological stress and amphetamine-induced dopamine release in the striatum (Wand et al. 2007). Another study reviewed that reward deficiency paralleled blunted reactivity to acute stress (Carroll et al. 2017). Moreover, reward and stress processing share the same brain circuit of frontal-limbic areas, which are concerned with both motivated behavior and autonomic regulation. Thus, individuals with a less efficient dopaminergic system may also
be characterized by a less efficient response to acute stress.
Elliot and colleagues theorized that the fundamentally central constructs of personality are two latent factors labeled as approach and avoidance
temperament, with neuroticism loading on avoidance temperament (Elliot and Thrash 2010). However, it was found that subjects with a high avoidance tendency show less neural activity than those with a high approach tendency during reward processing in the ventral striatum (Simon et al. 2010), which was also evidenced by our results in Chapter 5 that high motivated individuals valued reward much more than time (immediate versus delayed reward) in their decision making. Therefore, being loaded on avoidance temperament,
neuroticism may be related to a less efficient reward-motivation system. In light of this, the blunted acute stress response in high neuroticism that we observed in Chapter 2 probably signified a lower willingness to make effort in a
demanding situation. In addition, the experience of life-threatening events was also associated with increased avoidance motivation (Van Dijk et al. 2013), which may partially explain why a high frequency of stressful events was linked with a blunted response to acute stress in Chapter 3. Combining the possible role of dopamine with acute stress response - a mental preparation for one’s response, we speculate that the blunted acute stress response in individuals with high neuroticism and/or those with frequent exposure to stressful life events may be a manifest that the person was not primarily motivated to engage in self-protection but rather tried to avoid or withdraw in a stressful situation.
2.4 Conclusion
In sum, individual differences in acute stress responses are linked to several factors, but their underlying common source from a biological perspective is still unclear. We conclude that altered acute stress responses may be associated with hampered emotion processing related to higher amygdala reactivity, a weaker cognition and emotion regulation in frontal cortex, and an inefficient reward-motivation processing with dopamine activity related to active coping. Though we discussed these three possible
mechanisms separately above, in reality they are interrelated structurally and functionally. As proposed graphically in Figure 1, an integrated model may facilitate identifying individual differences in stress vulnerability and resilience.
Figure 1. The possible information-processing variables affecting individual differences in acute stress responses.
The three factors in the model adjust behavior through interaction with each other. For example, greater prefrontal executive control facilitates emotion regulation through reappraisal (Scult et al. 2017), whereas emotion and
motivation determine the affective significance of an event, which impacts attentional and effortful functions and further alters behavioral performance (Taylor et al. 2004; Pessoa 2009; Padmala et al. 2011). In fact, deficits in these three facets are found concurrently in many mental disorders such as
depression (Joormann and Michael Vanderlind 2014; Grahek et al. 2019) and schizophrenia (Barch 2005). Further, the three factors also interact strongly at the brain structure and function level. For example, DTI and neurotransmitter studies showed that the prefrontal cortex (deemed as the “cognitive brain”) communicates with subcortical key regions for emotion and reward processing via axonal and neurotransmitter projection to (or from) these regions (Arco and Mora 2009; Pessoa 2017). Moreover, prefrontal brain regions, such as lateral prefrontal cortex (LPFC), are involved in several functional networks
simultaneously featuring a high degree of connectivity (functional hubs), which are critical for regulating the flow and integration of cognition, motivation and emotion (for a review, Pessoa 2008). Lastly and foremostly, the stress response
is a dynamic process. When unexpected events occur, one’s emotional response to the individually perceived salience significance of the (potentially threatening) event may be generated in the amygdala. This may activate the motivation-reward dopamine system, which may then drive the individual to be proactive by prioritizing the reallocation of available resources to the stressor, or to react passively with autonomic but no overt behavioral responses. At the same time, a more flexible cognitive and emotional regulation capacity benefits individuals by continually updating the perceived affective significance,
selecting appropriate strategies and speeding up recovery from the stressful experience. Thus, it is proposed that these factors jointly determine how a person perceives, copes with and recovers from a stressor.
3 The dissociative effect of acute stress on reward anticipation
and reward consumption
Our findings in Chapter 4 showed that activity in the bilateral putamen during reward anticipation was greater in acute stress than in a neutral control situation, and that the dorsal striatum and right thalamus exhibited decreased activity during reward consumption under acute stress. We here discuss the mechanisms underlying the interaction between acute stress and reward processing more extensively.
The observed dissociation between reward anticipation and reward consumption is consistent with previous findings indicating a dissociation between the anticipation versus the consumption phase of reward processing at both the behavioral and the neural level. For instance, it was observed that participants mobilized more effort to choose reward cues in a
Pavlovian-Instrumental transfer test in stressful versus neutral conditions, but they did not report the reward as being more pleasurable (Pool et al. 2015a). A previous fMRI study found that stress increased striatal and amygdala activation during reward anticipation but decreased striatal activation during reward
consumption (Kumar et al. 2014). Regarding increased neural activation during reward anticipation under acute stress, a traditional explanation of the buffering effect is that reward pursuing could buffer stress-triggered aversive feelings with the hedonic pleasure of reward. A recent explanation by Pool et al. (2015b) proposed that stress-induced wanting is driven by habits and
Pavlovian motivational bursts, but not the possible buffering effect of reward. Combined with reduced reward consumption under acute stress observed in Chapter 4, we consider the second explanation as more probable.
4 Different effects on reward processing from acute stress and
allostatic load
In contrast to acute stress, chronic stress or stress-induced mental disorders seems to be linked to blunted activation during both reward
anticipation and consumption, such as major depressive disorder (Smoski et al. 2009; Olino et al. 2011). An explanation could be that acute stress is a short-term state with temporal changes in emotions, behaviors, and molecular signaling, whereas chronic stress or stress-related disorders are long-term conditions that may result in maladaptive behavioral disposition and biological changes. For healthy individuals, sufficient physiological and psychological responses to acute stress, such as the increased neural activation during reward anticipation under acute stress, are indices that the body is able to exert an intuitive effort to defend against the aversive situation. In contrast, individuals experiencing chronic stress may have limited resources to cope with the stress due to chemical changes in the brain resulting from long-term stress exposure. For example, studies showed that chronic stress causes HPA axis dysregulation, reduces dopaminergic transmission in the prefrontal cortex (Mizoguchi et al. 2008) and impairs prefrontal cortex structure and function (Mika et al. 2012; de Araújo Costa Folha et al. 2017).
Overall, our results from Chapter 4 suggest that reward anticipation and reward consumption are two distinct processes that are associated with different neural responses under acute stress. Further, they suggest blunted neural responses during reward processing during stress as a vulnerability factor for the development of stress-induced disorders.
5 Methodological considerations and future research
5.1 Stress stages: reactivity, recovery and aftermath of stressIt is important to note that the stress response is a multi-stage process, as diverse molecular signals are dynamically triggered during different stages of the stress response (Hermans et al. 2014). This difference in neurobiology of discrete stress stages was found to exert different effects on behavior and cognition. For example, we observed decreased neural activation during reward consumption during stress reactivity (= immediately after an acute stressor) in Chapter 4, whereas van Leeuwen et al. (2019) reported an
increased neural responses to reward consumption in a task performed 50 min after stress exposure. In line with this temporal difference, a further study reported lower rejection rates of ambiguous unfair offers 75 min later versus immediately after the stressor (Vinkers et al. 2013).
Recent studies have begun to account for the distinct stages of stress processing by dividing the stress response pathway into three stages of stress reactivity: reactivity to acute stress, recovery from the stress experience, and the aftermath (long-term effects) of acute stress. In light of these stages, studies using repeated stress induction (e.g., unpredictive electrical shocks at any time during a task) can be considered to investigate stress reactivity, whereas studies conducting tasks immediately after a stressor may cover both the reactivity and recovery stage, depending on the duration of the respective task. One study divided these two stages using the mean peak of cortisol response as a cut-off, which occurred at about 15 min after stress onset (Finch et al. 2019), another study used a more elaborated cutoff based on individual peak value to differentiate between stress reactivity and stress recovery (Fiksdal et al. 2019). Regarding the aftermath of stress, tasks were started at 50 min and 75 min after stress in some studies (van Leeuwen et al. 2019; Vinkers et al. 2013).
This new development to consider separate stress response stages provides a promising approach for a more thorough understanding of the difference mechanisms underlying and moderating individual stress responses. How fast people recover from acute stress, for instance, may be an important aspect of stress resilience, independent from one’s immediate stress reactivity. One study showed that higher emotional intelligence is positively related to faster recovery from acute stress, but was not related with stress reactivity (Lea
et al. 2019). However, most studies did not consider different stress stages as an influential factor that needs to be controlled, which may be due to
insufficient measurements or the resulting higher complexity in statistical methods. To better understand the dynamics of how acute stress influences cognition and behavior, it is recommended that future studies extend measurements, observing longer periods after stress induction, ideally measuring stress reactivity, stress recovery, and the aftermath stage separately.
5.2 Cortisol responders and non-responders (high-responders and low-responders)
The concepts in the field of stress as described in the Introduction were mostly defined from a qualitative perspective, such as uncertain, imbalance and cumulative prediction error. However, whether a stress induction is in force may need additional objective markers of stress responses, especially
increases in cortisol levels. To validate that stress was successfully induced, two different approaches were used in previous study: One kind of studies categorized participants into cortisol responders (peak minus baseline cortisol, e.g., >1.5nmol/l or 2.5nmol/l, or > an increased percentage of 15.5%) versus non-responders (below the thresholds above) with an exact cutoff threshold of cortisol reactivity (Miller et al. 2013; Walter et al. 2018). The other kind of studies, as the present Chapter 2 and 3, did not classify responders or non-responders but considered a group averaged cortisol response as validated stress induction. The classifying method has the advantage that it dissociates potentially heterogeneous groups and potentially provides more information, however, it is a posterior category per se and therefore a somewhat arbitrary distinction. From a methodological perspective, the second way may be more appliable in healthy individuals as it is normal for a large sample to have a continuous distribution from very small to strong cortisol responses (after removing outliers). We prefer reporting results from both approaches to show more comprehensive findings in the future.
5.3 Ecological measure of stress
The physical and psychological data collected five minutes pre-TSST in the laboratory was used as baseline in our design in Chapter 2 and Chapter 3. Though this is a generally used method, an ecologically valid baseline measurement would provide better accuracy. It may be more natural and elaborated to assess individuals’ stress experiences with a longitudinal
approach such as the economic momentary assessment (EMA) approach (Bolger et al. 2003). For example, we could measure participants’ heart rate and perceived stress severity three times daily for one week before the experiment day through portable heart rate monitor and smartphones, and to then use these data as an individual baseline. Likewise, continuing to collect data for several days after the acute stress manipulation would extend our understanding about the period of time individuals need to overcome certain stressors.
6 Conclusion
This thesis investigated individual differences in acute stress and the neural interactions among acute stress, reward processing and motivation. We showed that personality traits, stressful life experiences and cognitive capability influence the intensity of individual acute stress responses. In addition, we found neural reward processing to be linked to intrinsic motivation and this relationship to be moderated by acute stress. Future investigation of the relationships between various phenotypic predictors of individual responses to acute stress will further help to elucidate the fundamental biological
mechanisms that determine individual stress vulnerability and resilience. This will ultimately guide efforts towards prevention and treatment of stress disorders.
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