Motivation and emotion/Book/2017/Biological factors in emotional reactivity
How do biological factors influence emotional reactivity?
- 1 Overview
- 2 Emotional reactivity and the brain
- 3 How nurture effects nature
- 4 Real world applications
- 5 Conclusion
- 6 See also
- 7 References
- 8 External links
Have you ever heard someone described as “an emotional person”? Although happiness is an emotion, you probably do not picture an excitable, happy person when you hear this phrase. More likely, you picture a person who is easily upset, cannot control their emotions, or is sensitive to emotional events. In other words, you picture someone with negative affective style, poor emotion regulation, or who is highly emotionally reactive (Table 1).
Definitions of affective style, emotion regulation, and emotional reactivity.
|Affective style||Stable individual differences in emotion regulation and reactivity (Davidson, Jackson, & Kalin, 2000)|
|Emotion regulation||Deliberate or automatic processes used to suppress, maintain, enhance, or modify emotional reactions (Davidson, 2001)|
|Emotional reactivity||Ease of emotional activation, intensity, and persistence of responses (Nock, Wedig, Holmberg, & Hooley, 2008)|
Imagine you have failed a university course. The immediacy, intensity, and duration of your response represent emotional reactivity. If you are immediately overwhelmed by immense disappointment, and struggle to recover, you would score highly on a measure of emotional reactivity. Emotional reactivity can be studied using self-report, observational and physiological measures. The Emotional Reactivity scale (ERS; Nock et al., 2008), and the Perth Emotional Reactivity scale (PERS; Becerra, Preece, Campitelli, & Scott-Pillow, 2017) are self-report measures. Although positive and negative reactivity are often considered dichotomous, a dip in one does not necessarily correspond to a rise in the other; they are distinct dimensions (Becerra et al., 2017). The PERS differentiates between these dimensions, while the ERS does not (Becerra et al., 2017). Heart rate, skin conductance, and patterns of brain activation are measured to infer arousal (degree of activation), because emotional reactions are assumed to coordinated expressive, physiological, and experiential responses (Mauss, Levenson, McCarter, Wilhelm, & Gross, 2005).
This chapter explores the biological causes and correlates of emotional reactivity, and their implications. Biological theories of emotion propose a finite number of basic emotions based on neural substrates, innate universal expressions, and unique feeling-motivational states (Izard, 1992). Neural substrates are the primary focus of this chapter, followed by applied perspectives relating reactivity to genetic predisposition and psychological wellbeing. As most literature on emotional reactivity uses positive and negative valence as umbrella terms for variants of joy and interest, and variants of fear, disgust, sadness and anger respectively, this chapter will follow suit. Interestingly, Arnold’s foundational cognitive appraisal theory of emotion (1960) also supports bivalent categorisation, suggesting emotions result from subcortical appraisals of whether stimuli are beneficial or harmful. The underlying physiology of individual differences in emotional reactivity has important implications for understanding behaviour and improving psychological wellbeing.
Emotional reactivity and the brain
The brain is complex, and separating the neurological correlates of emotional reactivity and emotion regulation is challenging (Domes et al., 2010). Reaction and regulation seem sequential, however top-down and bottom-up emotional processes are bidirectional and difficult to differentiate. Keep in mind emotional reactions both affect and are affected by regulation.
The forebrain, comprising the cerebral cortex and the limbic system, is where most differences in emotional reactivity arise. The cerebral cortex is the outermost layer of the brain, and has distinct areas involved in movement, sensation, and executive functions. The limbic system is a subcortical collection of structures important for emotion and motivation, and receives information from both cortical and mid/hindbrain structures. See Figure 2 for a depiction of terms used to describe anatomical locations.
The prefrontal cortex (PFC) is the area of the cerebral cortex corresponding approximately to the forehead (Figure 3). The PFC exhibits cognitive control when information is conflicting or ambiguous, guiding behaviour based on prior learning and current goals (Miller & Cohen, 2001). Miller and Cohen’s model of cognitive control (2001), found that contextual cues from the PFC bias other regions towards enhanced or reduced reactivity to emotional stimuli, supporting its role in reactivity, beyond top-down regulation.
Consistent with the idea of stable PFC activity influencing emotional reactivity, the valence hypothesis suggests cortical asymmetry represents a diathesis, or predisposed valent-specific sensitivity to emotional stimuli (Wheeler, Davidson, & Tomarken, 1993). Lateralised dominance is proposed to bias reactivity of other brain regions, and reflect trait characteristics (Table 2). Left hemispheric dominance is associated with higher behavioural approach system (BAS) scores, and right with higher behavioural inhibition system (BIS) scores (Sutton & Davidson, 1997). BAS and BIS represent trait sensitivity to incentives or threats, and are associated with extroversion and neuroticism respectively (Carver & White, 1994). The valence hypothesis suggests these traits predict reactivity, supported by findings that left hemispheric dominance was associated with increased reactivity to a positive film, whereas right hemispheric dominance was associated with increased reactivity to a negative film (Wheeler et al., 1993). However, findings that right PFC inhibition enhances, rather than reduces attention to aversive stimuli (Berger, Domes, Balschat, Thome, & Höppner, 2017) are inconsistent with the valence hypothesis. Although emotional reactivity and BIS/BAS tendencies represented by cortical asymmetry are clearly related, it could be argued that sensitivity to potential incentives or threats are more accurately conceptualised as motivational than emotional tendencies.
Factors associated with left or right hemispheric dominance.
|Left hemispheric asymmetry||Right hemispheric asymmetry|
|Increased positive reactivity||Increased negative reactivity|
|Higher BAS scores||Higher BIS scores|
|Higher extroversion||Higher neuroticism|
The dorsolateral PFC (dlPFC) has connections with areas important for motor control and voluntarily shifting gaze (Miller & Cohen, 2001), consistent with its role in executing planned behaviours. This also reflects its involvement in approach and avoidance behaviours and representations of goal states. Imaging techniques have shown this region to be active in both up and down-regulation of emotional responses, likely suppressing distraction and maintaining focus on regulatory goals (Eippert et al., 2006). Stimulation increasing left dlPFC activity resulted in less time spent looking at threatening stimuli, thereby reducing reactivity (Chen, Basanovic, Notebaert, MacLeod, & Clarke, 2017), demonstrating how frontal regions proactively influence reactivity.
The ventromedial PFC (vmPFC) and orbitofrontal cortex(OFC) lie in the lower prefrontal region and contribute to top-down regulation of limbic regions (Hare et al., 2008; Eippert et al., 2006). During adolescence, the ventral PFC shows increased response to both happy and sad expressions, indicating its function is not valent-specific (Hare et al., 2008). The vmPFC may represent both positive and negative states in the absence of immediate incentives (Davidson & Irwin, 1999). Berridge and Kringelbach (2013) differentiate between representation and causation of emotion, concluding that prefrontal regions, particularly the OFC, are representative, rather than causal. While prefrontal regions may be necessary to consciously experience emotion, emotion does not originate from these regions, but from structures in the limbic system.
Anterior cingulate cortex
The anterior cingulate cortex (ACC) lies ventral to other cortical regions, and is highly connected to the limbic system. It is sometimes considered a prefrontal area (eg. Eippert et al., 2006), and is thought to connect the limbic system with the PFC, acting as “an interface between emotion and cognition” (Allman, Hakeem, Erwin, Nimchinksy, & Hof, 2001). This ACC regulates amygdala activity either directly, or by recruiting prefrontal regions to exhibit top-down control (Eippert et al., 2006).
The amygdala has been highlighted by cognitive (Arnold, 1960) and biological theorists, as essential in activating emotion. It is seen as an origin of emotional experience, and communicates with cortical structures, and lower brain regions involved in preparing the body to respond to threats (Arnsten, 2009). Although often associated with fear, the amygdala plays a broader role in determining whether a situation is harmful or beneficial (Yaniv, Desmendt, Jaffard, & Richter-Levin, 2004). Women, who are stereotypically more emotional than men, show greater amygdala reactivity in response to neutral stimuli (Domes et al., 2010); it is the appraisal of a stimulus as relevant to one's wellbeing, not the stimulus itself, that leads to emotion. Just as in cortical regions, amygdala lateralisation contributes to valent-specific affective sensitivity. Right amygdala dominance is associated with higher dispositional negative affect (Davidson & Irwin, 1999), while stronger left amygdala responses to happy faces are predicted by higher extroversion scores (Canli, Sivers, Whitfield, Gotlib, & Gabrieli, 2002).
The basal ganglia are highly connected subcortical structures relevant to emotional reactivity, inclucing the caudate nucleus and the nucleus accumbens (NAcc). The caudate nucleus, like the amygdala, is more reactive to positive stimuli in extroverts (Canli et al., 2001). This region is often associated with reward, or positive emotion, however this has been challenged by a study finding stronger caudate responses to negative than positive or neutral pictures (Carretie et al., 2009). The NAcc is now being investigated as an origin-point of emotion. A review by Berridge and Kringelbach (2013) supported the causal role of the NAcc in pleasure responses, describing a ‘keyboard mechanism’ for valence generation of hedonic like-dislike emotions. Specific locations or 'hedonic hotspot circuits' along the medial shell of the NAcc were found to trigger different mixtures of desire or fear, based on location, just as the location of keys on a keyboard determine the sounds resulting from playing (Berridge, & Kringelbach, 2013; Reynolds & Berridge, 2008).
Bringing it together
Different regions of the brain do not work in isolation, but use chemicals called neurotransmitters to form pathways and feedback loops. A stimulated neuron in one area releases a neurotransmitter, which may activate or inhibit neighbouring neurons. Those neurons then send excitatory or inhibitory messages to their neighbours, and so on. Perhaps you have heard simplified explanations of brain chemistry, such as 'dopamine causes pleasure' or, 'oxytocin causes love'. In reality, their roles are complex. For exampleː
- Oxytocin administration reduced fear-related amygdala activity among individuals with social anxiety (Labuschagne et al., 2010), and borderline personality disorder (Simeon et al., 2011), but did not cause them to fall in loveǃ
- Dopamine is involved in stress as well as pleasure, which may be better attributed to endorphins (Berridge & Kringelbach, 2013).
- Serotonin can be both anxiogenic and anxiolytic, depending on the type of receptor activated (Charney, 2004).
The bidirectional connections between the ventral PFC and the amygdala enable suppression of amygdala responses, and predict habituation to emotional stimuli (Hare et al., 2008) (Figure 3). During down-regulation of stress responses, prefrontal regions such as the OFC engage, reducing amygdala activity. During acute stress, the amygdala activates hypothalamic pathways which releases high levels of norepinephrine and dopamine, inhibiting PFC function and reducing capacity for down-regulation (Arnsten, 2009). Artificially reducing dlPFC activity also increased reactivity to aversive and neutral stimuli, through impairing regulatory capacity and indirectly disinhibiting the amygdala (Berger et al., 2017). This results in automatic responses based on salient features, rather than cognitive appraisal or goal-states (Arnsten, 2009).
How nurture effects nature
Epigenetic changes are changes in gene expression. Explained simply, experiences can switch genes on or off (Figure 4), enabling environmental factors to effect long-lasting physiological changes. Some people are more sensitive to environmental influence than others. Boyce and Ellis (2005) termed this 'biological sensitivity to context', and argued that high phenotypic reactivity may lead to negative outcomes in stressful settings, but also increase susceptibility to positive influences. Epigenetic processes adapt response systems to the environment they develop in; stress reactivity may reflect the placticity of stress response systems (Boyce & Ellis, 2005). The diathesis-stress model proposes that underlying vulnerability predisposes an individual to be adversely impacted by stressors. The differential susceptibility hypothesis is an alternative perspective which suggests individuals differ in plasticity, with highly reactive individuals disproportionately affected by enriching, and negative experiences (Belsky & Pluess, 2009), consistent with Boyce and Ellis' findings (2005).
Emotional reactivity and psychopathology
Increasingly, emotional reactivity is implicated in psychopathology. Exceptionally high and low reactivity is associated with poor psychological outcomes (eg. M’Bailara et al., 2009; Reichenberger, Wiggert, Agroskin, Wilhelm, & Blechert, 2017). Altered emotional reactivity is a feature of depression (Reichenberger et al., 2017), borderline personality disorder (Glaser, Os, Mengelers, & Myin-Germeys, 2008), and bipolar disorder, even during asymptomatic periods (M’Bailara et al., 2009). Further, emotional reactivity significantly explains the relationship between psychopathology and self-injurious thoughts and behaviours (Nock et al., 2008).
One version (polymorphism) of a gene involved in transporting serotonin (5-HTTLPR) is being investigated for its role in reactivity in mood disorders. The short polymorphism of this gene reduces serotonin availability, resulting in increased amygdala activity and decreased coupling between the amygdala and regulatory prefrontal areas (Hariri & Holmes, 2006). This polymorphism is thought to increase stress sensitivity, magnifying the risk of developing disorders including depression, anxiety and post-traumatic stress disorder (Caspi, Hariri, Holmes, Uher, & Moffitt, 2010).
Real world applications
By now you might be asking, “this is interesting, but how does it help me? Will knowing this stop me crying in cartoons or freaking out before exams?” The answer is probably not, but there are things you do everyday that impact your reactive tendencies for better or worse.
Why do things seem better in the morning?
You’ve probably heard that there’s nothing a good night’s sleep won’t fix. This may be an overstatement, but there is a biological explanation for why a seemingly insurmountable stressor may seem more approachable in the morning. During rapid eye movement (REM) sleep, amygdala responses to affective stimuli from the previous day become depotentiated (van der Helm et al., 2011). Amygdala activity is reduced during recall, prefrontal connectivity is re-established, and subjective emotional reactivity is reduced (van der Helm et al., 2011). This may be attributable to reduced adrenergic activity during REM sleep, or the benefit of REM sleep on emotional memory consolidation, which reduces stimulus novelty. Unfortunately, while REM sleep reduces emotional reactivity, reactivity can also reduce REM sleep quality. Deprivation of REM sleep increases emotional reactivity and prevents habituation to emotional stimuli (Rosales-Lagarde et al., 2012).
Other day-to-day influences
Self-control, mindfulness and environmental factors also alter emotional reactivity. According to the strength model of self-control, self-control is a limited resource and can be depleted through resisting short-term benefits in favour of long-term goals (Baumeister, Vohs, & Tice, 2007). Depletion of self-control also resulted in increased amygdala activity when repeatedly exposed to negative emotional scenes instead of habituation. (Wagner, & Heatherton, 2013). Depleated participants showed less vmPFC-amygdala connectivity than controls and increased amygdala activity in response to neutral scenes (Wagner, & Heatherton, 2013). This may be why after a stressful day in which you resisted yelling at your boss (short-term gain), to remain well-placed for promotion (long-term goal), you are more likely to go home and snap at your family. Luckily, if you do offend a loved one, they will likely be less upset the following day, after some REM sleep!
Appreciating little things is another way to boost wellbeing. ‘Flourishers’ (individuals with optimal mental health) are more reactive to pleasant events than others, and positive reactivity was predicted by mindfulness (Catalino, & Fredrickson, 2011). Mindfulness is beneficial to emotional reactivity for both beginners and experts, although skill level is associated with different patterns of neural activity (Taylor et al., 2011). For beginners but not experts, viewing emotional stimuli in a mindful state was associated with reduced left amygdala activity. Compared to beginners, experts showed relative deactivation of cortical areas. This may be because experts have learned to observe, rather than suppress experiences. Mindfulness attenuates chronic reactivity by replacing evaluation, or appraisal of affect, with sensory-based representations of emotion (Farb et al., 2010).
An alternative strategy for increasing positive and reducing negative reactivity, is to ‘tune’ the NAcc ‘keyboard’ by situating yourself in a preferred environment. Stressful environments expand fear-generating zones, whereas pleasant environments expand appetitive-generating zones (Reynolds & Berridge, 2008). In effect, being somewhere you like simultaneously decreases your potential for negative reactions and increases your potential for positive reactions.
Emotional reactivity is a small part of emotional experience with far reaching implications ranging from neuroplasticity to psychological wellbeing. The primary brain regions involved in emotional reactivity are the PFC and the limbic system. While cortical areas bias other regions towards particular response patterns, the amygdala and the NAcc contribute causally to emotional activation (Berridge & Kringelbach, 2013). High reactivity may reflect heightened sensitivity to positive and negative environmental factors, increasing susceptibility to epigenetic changes (Boyce & Ellis, 2005). While reactivity is implicated in psychopathology, it can be altered to improve psychological wellbeing through sleep management, mindfulness, and simply visiting your favourite place. Biological predispositions are not set in stone. Hopefully, understanding the biological processes underlying emotional reactivity will give you insight into your own tendencies, and empower you to take advantage of your brain's ability to change.
- Affect intensity (Book chapter, 2015)
- Cortical activation patterns and emotion (Book chapter, 2016)
- Emotional self-regulation (Book chapter, 2013)
Arnold, M. B. (1960). ‘’Emotion and personality, volume II: Neurological and physiological aspects.’’ New York: Columbia University Press.
Arnsten, A. F. (2009). Stress signalling pathways that impair prefrontal cortex structure and function. ‘’Nature Reviews. Neuroscience, 10’’, 410–422. http://doi.org/10.1038/nrn2648doi:10.1038/nrn2648. https://doi.org/10.1038/nrn2648
Baumeister, R. F., Vohs, K. D., & Tice, D. M. (2007). The strength model of self-control. ‘’Current Directions in Psychological Science, 16’’, 351-355. https://doi.org/10.1111/j.1467-8721.2007.00534.x
Becerra, R., Preece, D., Campitelli, G., & Scott-Pillow, G. (2017). The Assessment of Emotional Reactivity Across Negative and Positive Emotions: Development and Validation of the Perth Emotional Reactivity Scale (PERS). ‘’Assessment’’. https://doi.org/10.1177/1073191117694455
Belsky, J., & Pluess, M. (2009). Beyond diathesis stress: Differential susceptibility to environmental influences. ‘’Psychological Bulletin, 135’’, 885-908. https://doi.org/10.1037/a0017376
Berger, C., Domes, G., Balschat, J., Thome, J., & Höppner, J. (2017). Effects of prefrontal rTMS on autonomic reactions to affective pictures. ‘’Journal of Neural Transmission, 124’’, 139-152. https://doi.org/10.1007/s00702-015-1491-4
Berridge, K. C., & Kringelbach, M. L. (2013). Neuroscience of affect: Brain mechanisms of pleasure and displeasure. ‘’Current Opinion in Neurobiology, 23’’, 294–303. https://doi.org/10.1016/j.conb.2013.01.017
Boyce, W. T., & Ellis, B. J. (2005). Biological sensitivity to context: I. An evolutionary–developmental theory of the origins and functions of stress reactivity. ‘’Development and Psychopathology, 17’’, 271-301. https://doi.org/10.10170S0954579405050145
Carretie, L., Rios, M., de la Gandara, B. S., Tapia, M., Albert, J., López-Martína, S., & Álvarez-Linera, J. (2009). The striatum beyond reward: Caudate responds intensely to unpleasant pictures. ‘’Neuroscience, 164’’, 1615–1622. https://doi.org/10.1016/j.neuroscience.2009.09.031.
Canli, T., Sivers, H., Whitfield, S. L., Gotlib, I. H., & Gabrieli, J. D. (2002). Amygdala response to happy faces as a function of extraversion. ‘’Science, 296’’, 2191-2191. https://doi.org/10.1126/science.1068749
Canli, T., Zhao, Z., Desmond, J. E., Kang, E., Gross, J., & Gabrieli, J. D. (2001). An fMRI study of personality influences on brain reactivity to emotional stimuli. ‘’Behavioral Neuroscience, 115’’, 33. https://doi.org/10.1037/0735-7044.115.1.33
Caspi, A., Hariri, A. R., Holmes, A., Uher, R., & Moffitt, T. E. (2010). Genetic sensitivity to the environment: the case of the serotonin transporter gene and its implications for studying complex diseases and traits. ‘’Focus, 8’’, 398-416. https://doi.org/10.1176/appi.ajp.2010.09101452
Carver, C. S., & White, T. L. (1994). Behavioral inhibition, behavioral activation, and affective responses to impending reward and punishment: The BIS/BAS Scales. ‘’Journal of Personality and Social Psychology, 67’’, 319-333. https://doi.org/10.1037/0022-35184.108.40.2069
Catalino, L. I., & Fredrickson, B. L. (2011). A Tuesday in the Life of a Flourisher: The Role of Positive Emotional Reactivity in Optimal Mental Health. Emotion, 11, 938–950. https://doi.org/10.1037/a0024889
Charney, D. S. (2004). Psychobiological mechanisms of resilience and vulnerability. ‘’Focus, 2’’, 368-391. https://doi.org/10.1176/appi.ajp.161.2.195
Chen, N. T., Basanovic, J., Notebaert, L., MacLeod, C., & Clarke, P. J. (2017). Attentional bias mediates the effect of neurostimulation on emotional vulnerability. ‘’Journal of Psychiatric Research, 93’’, 12-19. https://doi.org/10.1016/j.jpsychires.2017.05.008
Davidson, R. J. (2001), Toward a Biology of Personality and Emotion. Annals of the New York Academy of Sciences, 935, 191–207. https://doi.org/10.1111/j.1749-6632.2001.tb03481.x
Davidson, R. J., & Irwin, W. (1999). The functional neuroanatomy of emotion and affective style. ‘’Trends in Cognitive Sciences, 3’’, 11-21. https://doi.org/10.1016/S1364-6613(98)01265-0
Davidson, R. J., Jackson, D. C., & Kalin, N. H. (2000). Emotion, plasticity, context and regulation: Perspectives from affective neuroscience. Psychological Bulletin, 126, 890-909. https://doi.org/10.1037/0033-2909.126.6.890
Domes, G., Schulze, L., Böttger, M., Grossmann, A., Hauenstein, K., Wirtz, P. H., ... & Herpertz, S. C. (2010). The neural correlates of sex differences in emotional reactivity and emotion regulation. ‘’Human Brain Mapping, 31’’, 758-769. https://doi.org/10.1002/hbm.20903
Eippert, F., Veit, R., Weiskopf, N., Erb, M., Birbaumer, N., & Anders, S. (2007). Regulation of emotional responses elicited by threat‐related stimuli. ‘’Human Brain Mapping, 28’’, 409-423. https://doi.org/10.1002/hbm.2029
Farb, N. A. S., Anderson, A. K., Mayberg, H., Bean, J., McKeon, D., & Segal, Z. V. (2010). Minding One’s Emotions: Mindfulness Training Alters the Neural Expression of Sadness. Emotion, 10, 25–33. https://doi.org/10.1037/a0017151.
Glaser, J., Os, J., Mengelers, R., & Myin-Germeys, I. (2008). A momentary assessment study of the reputed emotional phenotype associated with borderline personality disorder. ‘’Psychological Medicine, 38’’, 1231-1239. https://doi.org/10.1017/S0033291707002322
Hariri, A. R., & Holmes, A. (2006). Genetics of emotional regulation: the role of the serotonin transporter in neural function. ‘’Trends in Cognitive Sciences, 10’’, 182-191. https://doi.org/10.1016/j.tics.2006.02.011
Hare, T. A., Tottenham, N., Galvan, A., Voss, H. U., Glover, G. H., & Casey, B. J. (2008). Biological substrates of emotional reactivity and regulation in adolescence during an emotional go-nogo task. Biological Psychiatry, 63, 927-934. https://doi.org/10.1016/j.biopsych.2008.03.015015
Izard, C. E. (1992). Basic emotions, relations among emotions, and emotion-cognition relations. ‘’Psychological Review, 99’’, 561-565. http://doi.org/10.1037/0033-295X.99.3.561
Labuschagne, I., Phan, K. L., Wood, A., Angstadt, M., Chua, P., Heinrichs, M., … Nathan, P. J. (2010). Oxytocin attenuates amygdala reactivity to fear in generalized social anxiety disorder. ‘’Neuropsychopharmacology, 35’’, 2403–2413. http://doi.org/10.1038/npp.2010.123
Mauss, I. B., Levenson, R. W., McCarter, L., Wilhelm, F. H., & Gross, J. J. (2005). The tie that binds? Coherence among emotion experience, behavior, and physiology. ‘’Emotion, 5’’, 175-190. https://doi.org/10.1037/1528-35220.127.116.11
M’Bailara, K., Demotes-Mainard, J., Swendsen, J., Mathieu, F., Leboyer, M. and Henry, C. (2009), Emotional hyper-reactivity in normothymic bipolar patients. Bipolar Disorders, 11, 63–69. https://doi.org/10.1111/j.1399-5618.2008.00656.x.
Miller, E. K., & Cohen, J. D. (2001). An integrative theory of prefrontal cortex function. ‘’Annual Review of Neuroscience, 24’’, 167-202. https://doi.org/10.1146/annurev.neuro.24.1.167.
Nock, M. K., Wedig, M. M., Holmberg, E. B., & Hooley, J. M. (2008). The emotion reactivity scale: Development, evaluation, and relation to self-injurious thoughts and behaviors. Behaviour Therapy, 39, 107-116. https://doi.org/10.1016/j.beth.2007.05.005
Reichenberger, J., Wiggert, N., Agroskin, D., Wilhelm, F. H., & Blechert, J. (2017). No praise, please: Depressive symptoms, reactivity to positive social interaction, and fear of positive evaluation. Journal of Behaviour Therapy and Experimental Psychiatry, 54, 186-194. https://doi.org/10.1016/j.jbtep.2016.08.007
Reynolds, S. M., & Berridge, K. C. (2008). Emotional environments retune the valence of appetitive versus fearful functions in nucleus accumbens. ‘’Nature neuroscience, 11’’, 423-425. https://doi.org/10.1038/nn2061
Rosales-Lagarde, A., Armony, J. L., del Río-Portilla, Y., Trejo-Martínez, D., Conde, R., & Corsi-Cabrera, M. (2012). Enhanced emotional reactivity after selective REM sleep deprivation in humans: an fMRI study. Frontiers in Behavioral Neuroscience, 6, 25. https://doi.org/10.3389/fnbeh.2012.00025
Simeon, D., Bartz, J., Hamilton, H., Crystal, S., Braun, A., Ketay, S., & Hollander, E. (2011). Oxytocin administration attenuates stress reactivity in borderline personality disorder: a pilot study. ‘’Psychoneuroendocrinology, 36’’, 1418-1421. https://doi.org/10.1016/j.psyneuen.2011.03.013
Sutton, S. K., & Davidson, R. J. (1997). Prefrontal brain asymmetry: A biological substrate of the behavioral approach and inhibition systems. ‘’Psychological Science, 8’’, 204-210. https://doi.org/10.1111/j.1467-9280.1997.tb00413.x
Taylor, V. A., Grant, J., Daneault, V., Scavone, G., Breton, E., Roffe-Vidal, S., ... & Beauregard, M. (2011). Impact of mindfulness on the neural responses to emotional pictures in experienced and beginner meditators. Neuroimage, 57, 1524-1533. https://doi.org/10.1016/j.neuroimage.2011.06.001.
Van der Helm, E., Yao, J., Dutt, S., Rao, V., Saletin, J. M., & Walker, M. P. (2011). REM sleep depotentiates amygdala activity to previous emotional experiences. Current Biology, 21, 2029-2032. https://doi.org/10.1016/j.cub.2011.10.052
Wagner, D. D., & Heatherton, T. F. (2013) Self-regulatory depletion increases emotional reactivity in the amygdala. Social Cognitive and Affective Neuroscience, 8, 410–417. https://doi.org/10.1093/scan/nss082.
Wheeler, R. E., Davidson, R. J., & Tomarken, A. J. (1993) Frontal brain asymmetry and emotional reactivity: A biological substrate of affective style. Psychophysiology, 30, 82-88. https://doi.org/10.1111/j.1469-8986.1993.tb03207.x
Yaniv, D., Desmedt, A., Jaffard, R., & Richter-Levin, G. (2004). The amygdala and appraisal processes: stimulus and response complexity as an organizing factor. ‘’Brain Research Reviews, 44’’, 179-186. https://doi.org/10.1016/j.brainresrev.2003.08.008
- Glossary of Psychological Terms (American Psychological Association)
- Perth Emotional Reactivity Scale (PERS): Questionnaire and scoring instructions (researchgate.net)