Motivation and emotion/Book/2017/Norepinephrine and emotion

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Norepinephrine and emotion:
What is the relationship between norepinephrine and emotion?


Norepinephrine, or noradrenaline, is a catecholamine synthesised from dopamine by dopamine ß-hydroxylate, that acts as both a hormone and a neurotransmitter (Nagatsu, Levitt, Udenfriend, 1964). It works in postganglionic neurons in the brain as a neurotransmitter (sympathetic nervous system) (Moret & Briley, 2011). It is found in multiple parts of the brain, however most projections are from the Locus Coerulus and the Lateral Tegmented Nuclei, which are found throughout the ventral pons and the medulla (Ressler & Nemeroff, 2000). Norepinephrine is known to be a major contributor in the fight or flight response to internal and external stressors, this is because of the multitude of effects norepinephrine has on the body when an individual experiences stress (Koob, 1999). Norepinephrine has also been shown to have a relationship with various other emotions including fear (Johnson, Hou, Prgaer & LeDoux, 2011) (Schachter, 1957) (White & Depue, 1999), lust, attraction and attachment (Fisher, 2000), and pain and anger (Schachter, 1957). Not only this, but Norepinephrine plays a role in the perception of emotional expression (Harrison, Morgan & Critchley, 2010). Norepinephrine has also be found to play an important role in mood disorders, such as depression and anxiety (Moret & Briley, 2011). This finding lead to the production of Selective Norepinphrine[spelling?] Reuptake Inhibitors (SNRI's), a medication used in the treatment of depression (Brunello, Mendlewicz, Kasper,, Leonard, Montgomery, Nelson, Paykel, Versiani & Racagni, 2002).

The following questions will be addressed in this chapter.

  • What is Emotion and what are the main theories of emotion?
  • What is Norepinephrine and how does it work?
  • What effects does Norepinephrine have on emotion?

Theories of emotion[edit]

Emotion is a concept that has been widely researched and a number of theories have been developed in the area. Emotion is more than just our feelings, it also relates to bodily-arousal and physiological mechanisms that pair with our thoughts and feelings, as well as how we express our emotions and how we perceive others' emotional expressions (Harrison, Morgan & Critchley, 2010). Theories of emotion are categorised into three main sub sections, evolutionary (genetic/innate), physiological (physical reactions), and cognitive (mental/mind reactions).


Ekman's argument for basic emotions (Ekman, 1992)

Paul Ekman developed the idea that there are six basic emotions. He believed that these basic emotions were the central themes in emotion families, that other emotions were related to or shared common themes with one of the basic six. They are basic because of their innate nature and because they are used to deal with fundamental life tasks that are seemingly timeless and universal.

Ekman's proposed six basic emotions are:

  • Fear
  • Anger
  • Disgust
  • Sadness
  • Interest
  • Joy

He proposed that these basic emotions have nine shared characteristics:

  1. Distinctive Universal Signals: e.g. a unique facial expression
  2. Presence in other primates: e.g. similar expression in other primates
  3. Distinctive Physiology: e.g. specific physiological responses
  4. Distinctive universals in antecedent events: e.g. consistent across cultures and context
  5. Coherence among emotional response: e.g. responses relate to one another
  6. Quick onset: e.g. begin quickly
  7. Brief duration: e.g. end quickly
  8. Automatic appraisal: one of two mechanisms, either automatic (capable of operating at great speed) or extended (cognition needed to determine emotion)
  9. Unbidden occurence[spelling?]: e.g. we cannot not determine the emotions we feel


James-Lange Theory (Cannon, 1987)

The James-Lange theory was developed by William James and Carl Lange in 1922 in their publication 'The Emotions'. Basically, the scholars proposed that emotion comes as a result of physiological arousal. That is, that we experience emotion after our bodies physiological responses have taken place. Lange believed that the vasomotor system was the root of all emotional affect, while James felt that emotions were just the feeling of changes in the body. Both scholars had similar thoughts on the theory behind emotion independently but at similar times. The basis of this theory has been largely criticised in more recent research, partly due to progressive research that was not around when James and Lange were developing their theory. The whole idea that physiological changes come before emotional experience has been criticised, but so too has the specific details of both James's and Lange's proposals for the exact procedure for emotional experience.

Cannon-Bard Theory (Cannon, 1987)

The Cannon-Bard Theory was developed by Walter Cannon and his doctoral student Philip Bard. The two had substantial criticisms of the James-Lange Theory, and so they developed an alternative theory for the physiological theories of emotion. The theory is commonly referred to as the Thalamic Theory of Emotion because the two proposed that expression of emotions and the feeling of emotions resulted from hypothalamic structures, in particular the dorsal thalamus in regards to emotional feelings.

Schachter-Singer Theory (Reisenzein, 1983)

The Schachter-Singer Theory of Emotion was developed by Stanley Schachter and Jerome Singer in 1962. The theory is also commonly known as the two-factor theory of emotion. The two believed that emotion came as a result of two factors, physiological arousal and a cognitive labelling of the said arousal. These two factors are both necessary for emotion, both are required and if one is missing there will be no emotion experienced. This has been criticised in more current research, proposing that there are not the only two factors needed to create the experience of an emotion.


Lazarus's Theory of Emotion (Smith & Lazarus, 1990)

Richard Lazarus developed the cognitive appraisal theory of emotion. This theory proposes that there is a cognitive aspect in the experience of emotions. Lazarus believed that in the case of an emotionally significant event, there are 3 steps.

  1. Cognitive Appraisal: The individual evaluates the event
  2. Physiological Response: The body reacts
  3. Action/Emotion: The individual experiences an emotion and determines their reaction to the event

On top of the cognitive appraisal theory, Lazarus also published literature regarding what he believed to be the five core emotions. These were:

  1. Anger
  2. Fear
  3. Sadness
  4. Disgust
  5. Happiness

Lazarus believed these five emotions shared core themes. They are very similar to the six emotions proposed by Ekman (1992), you could say interest and joy have been combined into happiness.

Test your knowledge[edit]

Which two of Ekman's basic emotions were left out of Lazarus's core emotions?

Interest and Joy
Interest and Disgust
Joy and Sadness
Sadness and Disgust

What are the two factors in Schichter and Singers Two Factor Theory?

Physiological arousal and cognitive labelling
Physiological labelling and cognitive arousal
Mental arousal and physical labelling
Mental labelling and physical arousal

Norepinephrine and emotion[edit]

Figure 1: Norepinephrine Molecule

The exact role norepinephrine plays in emotion is yet to be agreed upon. Emotion is such a large area of research, resulting in countless [vague] studies into all aspects of the field. It has been suggested that norepinephrine selectively enhances the firing of the neurons responsible for receiving external input for affective events, which in turn helps to create memories for such events[factual?]. This is known as the Kety Hypothesis (Harley, 1987). Numerous studies have reported the highest density of norepinephrine producing neurons can be found in the Locus Coerulus, a nucleus of the pons in the brain stem (Moret & Briley, 2011) (Brunello et. al, 2002) (Leonard, 2001) (Koob, 1999) (White & Depue, 1999) ( Ressler & Nemeroff, 2000) (Gu, Wang, Wang & Huang, 2016). It is known that from the Locus Coerulus, Norepinephrine is projected to various areas of the brain, inducing varying effects. For example, projections of norepinephrine into the limbic system, the emotional centre of the brain, helps to regulates emotion (Moret & Briley, 2011).


Figure 2: Norepinephrine's Pathway in the Brain

Stress, fear, anger and arousal have been shown to trigger norepinephrine (Johnson et al., 2011) (Schachter, 1957), as well as arousal, learning, memory, and sleep (Brunello et al., 2002). Stress triggers the projection of norepinephrine from the locus coerulus which leads to a release of norepinephrine in the central nervous system activating the hypothalamic-pituitary-adrenal axis (Leonard, 2001) (Gu et al., 2016). Stress increases the turn over of norepinephrine in the locus coerulus, increases extracellular norepinephrine in the hippocampus and induces the release of norepinephrine into the paraventricular nucleus of the hypothalamus, the bed nucleus of the stria terminalis, and the central nucleus of the amygdala (Koob, 1999). Stress and fear increases central and peripheral norepinephrine projections through synthesis, release and catabolism (White & Depue, 1999). Romantic attraction has also been seen to have a relationship with norepinephrine, triggering an increases of dopamine and norepinephrine and a decrease of serotonin in the brain (Fisher, 1957). Norepinephrine also induces a positive perception bias meaning that increased levels of norepinephrine will result in recognition of more positive emotions in other people (Harrison et al.,2010).

Depression and anxiety[edit]

Norepinephrine has shown to play an important role in mood disorders such as depression and anxiety (Moret & Briley, 2011). In some cases, depression and anxiety is caused due to a complete dysregulation of norepinephrine (Ressler & Nemeroff, 2000). The catecholamine theory of depression proposes that depression occurs due to norepinephrine deficiencies in the brain. That is to say that depletion of norepinephrine results in decreased mood, whereas an increase in the availability of norepinephrine leads to increased mood (Brunello et al., 2002).


Antidepressants work by increasing the concentration of neurotransmitters in the brain by either inhibiting the re-uptake or by inhibiting the degradation of the neurotransmitter (Brunello et al., 2002). In the same way that selective serotonin re-uptake inhibitors (SSRI's) are used to treat the serotonin pathway in depression, selective norepinephrine re-uptake inhibitors (SNRI's) work to treat the norepinephrine pathway in depression. Whilst this is still a somewhat new medication, it is proven to be an effective treatment option (Brunello et al., 2002). In fact, some studies have found SNRI's to be just as effective as SSRI's (Harley, 1987) (Brunello et al., 2002). SNRI's have also be shown to be effective in modulating the perception of emotional expression in others. A single dose of SNRI's is enough to cause positive emotional expression classification in healthy populations. Not only that, but SNRI's can also decrease the recognition of fearful and angry facial expressions. This is done by increasing the positive expression bias and decreasing the negative expression bias. In mood disorders such as depression and anxiety, individuals can have an increase in their negative expression bias, meaning that they may perceive negative emotions in others even when they are not present (Harmer, Shelley, Cowen & Goodwin, 2004). In the case of anxiety, research is not as abundant as it is for depression. Having said that, the efficacy of SNRI's on anxiety and panic disorders encourages the idea that norepinephrine has an important role in anxiety too (Brunello et al., 2002). SNRI's have also been used to treat Post Traumatic Stress Disorder (PTSD) due to norepinephrine's role in fear memories (Johnson et al., 2011).

Practical examples of SNRI's can be found here on the Beyond Blue online forum page.

Test your knowledge[edit]

The highest density of norepinephrine producing neurons can be found in which structure?

Locus Coerulus
Prefrontal Cortex
The Limbic System

The Catecholamine Theory proposes which of the following?

Depression occurs due to norepinephrine depletion
Depression occurs due to increased norepinephrine
Schizophrenia occurs due to increased norepinephrine
Depression occurs due to SNRI's


Overall, there is a clear relationship between norepinephrine and emotion. After understanding emotion more thoroughly through the use of the theories of emotion, it is clear that norepinephrine is involved in many important aspects of emotion[vague]. The multitude of physiological mechanisms by which norepinephrine acts are diverse [vague] and help to show just how much norepinephrine impacts on emotion. Norepinephrine also proved to be a big player when it comes to depression, SNRI's have proven to be an effective treatment method for depression as well as anxiety and panic disorders[grammar?]. Current research in the area is abundant, and future research will only continue to clarify norepinephrine's role as well as propose new theories as to how norepinephrine works[vague]. It would be beneficial to understand exactly what cognitive as well as physiological changes take place due to norepinephrine activity from internal and external stimuli, to help bridge the gap between evolutionary, physiological and cognitive emotion theories.

See also[edit]


Brunello, N, Mendlewicz, J, Kasper, S, Leonard, B, Montgomery, S, Nelson, J C, Paykel, E, Versiani, M & Racagni, G. (2002). The role of noradrenaline and selective noradrenaline reuptake inhibition in depression. European Neuropsychopharmocology, 12(5), 461-475.

Cannon, W. (1987). The James-Lange Theory of Emotions: A Critical Examination and an Alternative Theory. The American Journal of Psychology, 100(3/4), 567-586. https://doi:10.2307/1422695

Ekman, P. (1992). An argument for basic emotions. Cognition and Emotion, 6(3/4), 169-200.

Fisher, H. (2000). Lust, attraction, attachment: biology and evolution of the three primary emotion systems for mating, reproduction, and parenting. Journal of Sex Education and Therapy, 25(1), 96-104.

Gu, S., Wang, W., Wang, F. & Huang, J. (2016). Neuromodulator and emotion biomarker for stress induced mental disorders. Neural Plasticity, 2016, 1-6.

Harley, C. (1987). A role for norepinephrine in arousal, emotion and learning?: Limbic modulation by norepinephrine and the Kety hypothesis. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 11(4), 419-458.

Harmer, C., Shelley, N., Cowen, P. & Goodwin, G. (2004). Increased positive versus negative affective perception and memory in healthy volunteers following selective serotonin and norepinephrine reuptake inhibition. American Journal of Psychiatry, 161, 1256-1263.

Harrison, N., Morgan, R. & Critchley, H. (2010). From facial mimicry to emotional empathy: a role for norepinephrine?. Journal of Social Neuroscience, 5(4), 393-400.

Johnson, L., Hou, M., Prager, E. & LeDoux, J. (2011). Regulation of the fear network by mediators of stress: norepinephrine alters the balance between cortical and subcortical afferent excitation of the lateral amygdala. Frontiers in Behavioural Neuroscience, 5(23), 1-7. 10.3389/fnbeh.2011.00023 https://doi: 10.3389/fnbeh.2011.00023

Koob, G. (1999). Corticotropin-releasing factor, norepinephrine, and stress. Biological Psychiatry, 46(9), 1167-1180.

Leonard, B. (2001) Stress, norepinephrine and depression. Journal of Psychiatry and Neuroscience, 26, S11-6.

Moret, C & Briley, M. (2011). The importance of norepinephrine in depression. Neuropsychiatric Disease and Treatment, 7(1), 9-13.

Nagatsu, T., Levitt, M. & Udenfriend, S. (1964). Tyrosine Hydroxylase. The Journal of Biological Chemistry, 239(9), 2910-2917.

Reisenzein, R. (1983). The schachter theory of emotion: two decades later. Psychological Bulletin, 94(2), 239-264.

Ressler, K. & Nemeroff, C. (2000). Role of serotonergic and noradrenergic systems in the pathophysiology of depression and anxiety disorders. Depression and Anxiety, 12, 2-19.

Schachter, J. (1957). Pain, fear, and anger in hypertensives and normotensives. Psychosomatic Medicine, 19(1), 17-29.

Smith, C. & Lazarus, R. (1990). Emotion and Adaptation. Handbook of Personality: Theory and Research, 609-637.

White, T. & Depue, R. (1999). Differential association of traits of fear and anxiety with norepinephrine- and dark-induced pupil reactivity. Journal of Personality and Social Psychology, 77(4), 863-877.

External Links[edit]