Motivation and emotion/Book/2013/Dopamine and emotion
What is the role of dopamine in emotion?
How are you feeling today? Are you feeling happy for being productive today? Are you frustrated over not being able to watch the latest episode of your favorite TV series? Are you upset over someone’s behavior? Are you motivated to make a change in your lifestyle today? Emotions comprises of observable behaviors, expressed feelings and physiological changes in individuals.
There are four aspects to emotions: feelings, actions, physiological arousal, and motivation. Feelings are subjective and they consist of the states of what the individuals feel or experience (Breedlove et al., 2010). Actions in emotions involve the act acted upon the emotions, usually deemed as ‘emotional’.
For example, being defensive over an accusation or laughing at a joke. Physiological arousal is related to the emotions that we experience (Breedlove et al., 2010). The distinctive somatic and autonomic responses along with the behavior can be studied objectively on animals’ emotions. The aspect of motivation in emotions enables humans to adapt progressively (Breedlove et al., 2010).
There are two main classes of neurotransmitters known as monoamines: catecholamines and indoleamines. Catecholamine neurotransmitters, a type of amino acid tyrosine, consist of dopamine, epinephrine and norepinephrine (Breedlove, Watson, & Rosenzweig, 2010). Approximately a million nerve cells in the human brain contain dopamine. The subtypes of dopamine receptors had been labeled as D1, D2, D3, D4, and D5, according to the order of when these receptors were discovered (Breedlove et al., 2010).
Dopamine is a monoamine neurotransmitter located in the midbrain and basal forebrain that transmits signals in between the neurons of the brain, which aids the control centre of the brain in rewards and pleasure (Psychology Today, n.d.). Dopamine plays a role in regulation of movement and emotional responses whereby it allows human to perceive rewards and to act in accordance to the rewards. Deficiency in dopamine often results in Parkinson’s disease and it is known that low dopamine activity often causes addiction in individuals (Psychology Today, n.d.).
Some type of dopamine receptor is associated with sensation-seeking. When an individual experiences something pleasant that occurs unexpectedly, this activates the ventral tegmental area dopamine neurons. In the role of drugs and their addictive properties, it could possibly be caused by the release of dopamine in drug abuse (Newton, 2009). Lacking dopamine in the system may possibly cause mental retardation in cases of rare genetic diseases such as PKU and cretinism.
However, it should be noted that having high levels of dopamine can make an individual psychotic (Dean, 2011). As mentioned before in cases of drug abuse, drugs such as cocaine and methamphetamines cause the release of dopamine by inhibiting its reuptake. This is why high levels of dopamine lead to aggression, euphoria, and intense sexual feelings (Deans, 2011).
Relevant theories of emotion and bodily changes
There are several theories that had attempted to explain the relationship between emotions and activity of visceral organs that are controlled by the autonomic nervous system.
An American psychologist, William James (1842-1910) had suggested that bodily changes are the cause of emotion that humans experience. This theory was supported by Danish physician Carl G. Lange (1834-1900), who focuses on peripheral physiological event, whereby the perception of emotion is regulated by the autonomic nervous system. For example, when humans experience emotions such as happiness, based on the theory, it is caused by a certain stimuli perceived by the body which results in the emotion. Thus, it can be said that different emotions are produced by different yet distinctive psychological responses (Breedlove et al., 2010). The James-Lange theory had been considered in many attempts to connect human responses to emotions but many researches had shown that the theory does not have a substantial evidentiary explanation to the relationship. However, it does raise an idea of how emotions are related to the state of an individual’s body (Breedlove et al., 2010). In cases where people who suffered from spinal cord injuries had reported that they are unable to experience intense emotions with the assumption of the absence of sensory signals in their body (Hohmann, 1966).
This theory had been developed by physiologists, Walter Cannon (1871-1945) and Philip Bard (1898-1977), to challenge the James-Lange theory. They argued that the emotions are most likely to take place before any changes can take place in the autonomic nervous system, with an explanation that the relay of signals in the autonomic nervous system takes a longer time for changes to occur (Breedlove et al., 2010). Cannon explained that bodily responses are a form of emergency response of organisms when threatened, in the activation of the sympathetic nervous system which prepares the individual for ‘fight or flight’ (Cannon, 1929). The role of emotions was explained to prepare the organisms in dealing with the changes in environment. Cannon and Bard viewed that the brain decides on which emotion is suited as a response to the stimuli (Breedlove et al., 2010). This is explained that the cerebral cortex controls the emotional responses and the activation of the sympathetic system, to prepare the body for any action. Several researches on the effect's Cognitive Theory=== Stanley Schachter (1975) presented that emotions are nonspecific feelings of physiological arousal, and is influenced by the internal cognitive system, which deciphers and arrange the status of social, physical, and cognitive situations, in order to place appropriate labels to the emotion. In a renowned experiment conducted by Schachter and Singer (1962), participants were administered with epinephrine (adrenaline) and they were informed that no effect will take place. This group of participants reported the lack of emotional responses. However, in another group of participants whereby they’re not warned beforehand, experienced some form of emotion when the drugs reacted with their system (which supports James-Lange theory but not Cannon-Bard theory) (Breedlove et al., 2010). However, it should be noted that the emotion experienced is influenced by the emotions of other associates in the room (angry or happy). The participants injected with epinephrine were more likely to report the feeling of anger when an ‘angry’ associate is in the room or more likely to report a happy feeling when a ‘happy’ associate is present (Breedlove et al., 2010). The findings from the experiment showed that the interaction between physiological arousal and cognitive mechanisms results in an emotional state. However, Schachter's theory had been criticized that it only shows that physiological arousal is nonspecific and that it only affects the intensity of emotions but not the quality of it (Breedlove et al., 2010). Despite that, it was viewed that autonomic patterns differs in different emotions (Levenson, Ekman, & Friesen, 1990). The formulation on types of emotions experienced by human was developed by Plutchik (1994) whereby there are eight basic emotions¬; joy vs. sadness, affection vs. disgust, anger vs. fear, and expectation vs. surprise.
The role of dopamine in emotion
Negative emotional stimuli
Although the roles of dopamine in human emotion still remain unclear, studies that have been conducted on this aspect had shown that dopamine is responsible in the relay of positive and negative emotions.
A recent literature had discussed on the relationship of dopamine to aversive stimuli (Patin & Hurlemann, 2011). There are several studies conducted in attempt to test the effect of dopamine on neural processing of aversive stimuli. It was reported that with the introduction of dopamine agonist L-DOPA during an emotion matching task, there was a notable reduction in the right amygdale activity (Delaveau, Salgado-Pineda, Micallef-Roll, & Blin, 2007). In a similar experiment, researchers found an increase of amygdala responses to fear and angry facial expressions when amphetamine (0.25 mg/kg body weight) was induced (Hariri, Mattay, Tessitore, Fera, Smith, & Weinberger, 2002).
In another research, the effect of a 25-mg single oral dose of sultopridem (a dopamine D2/D3 receptor antagonist) was shown in the reduction of the activity in the left amygdala when unpleasant images were presented (Takahashi, Yahata, Koeda, Takano, Asai, Suhara, & Okubo, 2005). Results from these researches support the findings in the role of dopamine (D1) agonism in the reduction of fear-related emotions. Evidentiary support based on studies conducted on animal (Davis, Falls, Campeau, & Kim, 1993) and human (Aldhafeeri, Mackenzie, Kay, Alghamdi, & Sluming, 2012; Buchanan, Tranel, & Adolphs, 2004; Funamaya, Grillon, Davis, & Phelps, 2001), had shown the potential of aversive stimuli which is controlled by the amygdala—packed with dopamine receptors (Missale, Nash, Robinson, Jaber, & Caron, 1998), under the influence of dopamine transmissions (Kroner, Rosenkranz, Grace, & Barrionuevo, 2005). Corr and Kumari (2013) suggested two plausible explanations to these findings; d-amphetamine is related to fear related processes, or the effect as a secondary result to a primary effect on pleasure related processes, which provides a probable support to neurochemical and neurophysiological hyperactivity in mesolimbic dopamine reward system, in psychopathic individuals (Buckholtz, Treadway, Cowen, Woodward, Benning, Li, Ansari, Baldwin, Schwartzman, Shelby, Smith, Cole, Kessler, & Zald, 2010). This leads to the linkage between dopamine (amphetamine) and crimes, when drugs are abused (Fridell, Hesse, Jaeger, & Kuhlhom, 2008).
It was estimated that most crimes committed in the United States are conducted by offenders who abuses drugs (Miller, Levy, Cohen, & Cox, 2006). In the context of hyperdopaminergic activity, individuals who are vulnerable to reduced aversive motivation are more likely to be antisocial or to develop psychopathic personalities (Corr & Kumari, 2013). Negative emotional stimuli does not lead to the release of dopamine in the ventral striatum (Badgaiyan, 2010), which is why Parkinson’s patients often faces difficulties in processing negative emotions, but not positive emotions (Dara, Monetta, Pell, 2008). The processing of negative emotions is said to be linked to the release of dopamine in the amygdala, prefrontal and medial temporal areas (Badgaiyan, Fischman, & Alpert, 2009).
When individuals are in love, they perceive their beloved as unique, and their view on love are bounded with a "special meaning" (Tennov, 1979). The phenomenon of love is accompanied for the element of exclusivity. In the central nervous system, high concentrations of dopamine are linked to love (Tassin, Herve, Blanc, & Glowinski, 1980) alongside attention, motivation and goal-directed behaviors (Kiyatkin, 1995; Salamone, 1996; Scatton, D’Angio, Driscoll, & Serrano, 1988). It is suggested that levels of dopamine in the CNS rises in individuals who are in love when such emotions takes on to a ‘special meaning’. In addition, the ability to focus, remember, cherish of a beloved indicates that dopamine is involved in this phenomenon (Fisher, 2000).
Increased levels of dopamine had indeed been linked to undivided attention (Kiyatkin, 1995; Salamone, 1996; Scatton et al., 1988) whereas the role of norepinephrine had been linked to the increased memory for new stimuli (Griffin & Taylor, 1995). High concentrations of dopamine in the brain had also been associated with euphoria (Wise, 1988), loss of appetite (Colle & Wise, 1988), hyperactivity (Post, Weiss & Pert, 1988), increased mental activity, less likely to feel fatigue, the lack of need to sleep (Kruk & Pycock, 1991), ‘hyperactive fear-like state’ (Lee, Ellinwood & Nishita, 1988), anxiety and panic (Post, Weiss, & Pert, 1988).
Therefore, dopamine is most likely to be responsible for exhilaration, heightened energy, sleeplessness, reduced appetite, fear, anxiety that are connected the emotional system of love in humans. Individuals who are in love reported emotional dependency on the beloved and such feelings includes possessiveness, jealousy, fear of rejection and anxiety when separated (Fisher, 2000).
Dopamine deficiency in schizophrenic patients
In the studies of functional neuroimaging of schizophrenic patients, it was found that schizophrenic patients have dysfunctional limbic system—in the amygdala complex and frontal areas of the brain (Salgado-Pineda, Delaveau, Blin, & Nieoullon, 2005). It was found that there is an association in deficits when it comes to the identification of emotions with cognitive performances, and researches have reported a correlation between the deficiency in emotional discrimination tasks and performance on tasks of abstraction, memory, language, and executive and visuospatial functions (Schneider, Gur, Gur, et al., 1995; Bryson, Bell, & Lysaker, 1997; Whittaker, Deakin, & Tomenson, 2001). Schizophrenic patients with a dominance of negative symptoms exemplifies an inability in the recognition of negative emotions, whereas patients with positive symptoms had failed to recognize positive emotions (Mandal, Jain, Haque-Nizamie, et al. 1999).
In the frontal lobe, dopamine controls the transmission of signals from other areas in the brain. The frontal lobe consists of the limbic sections and lesions to the anterior cingulate gyrus are known to be associated to the impairment of emotional expression (Salgado-Pineda et al., 2005). MRI studies conducted on the brain have shown that the frontal area of the brain is more prone to injury (Levin, Amparo, Eisenberg, et al., 1987). Patients who suffered from traumatic brain injury are incapable of perceiving emotions in faces (Green, Turner, & Thompson, 2004).
The role of dopamine still remains unclear. However, there are recent studies that had supported the original theories on emotions and bodily changes. The levels of dopamine in the human body influences negative and positive emotions in individuals. The effects of dopamine in the human body (alongside other causes) are evidential in cases of patients suffering from schizophrenia, brain injuries, ADHD, Parkinson's disease and many more. Aside from that, dopamine in the brain enables us to perceive emotions in faces as well.
Aldhafeeri, F. M., Mackenzie, I., Kay, T., Alghamdi, J., & Sluming, V. (2012). Regional brain responses to pleasant and unpleasant IAPS pictures: different networks. Neurosci Lett, 512, 94–98.
Badgaiyan, R. D. (2010). Dopamine is released in the striatum during human emotional processing. Neuroreport, 21(18), 1172–1176.
Badgaiyan, R., Fischman, A., & Alpert, N. (2009). Dopamine release during human emotional processing. Neuroimage, 47, 2041–2045.
Breedlove, S. M., Watson, N. V., & Rosenzweig, M. R. (2010). Biological psychology: An introduction to behavioral, cognitive, and clinical neuroscience. Sunderland: Massachusetts: Sinauer Associates Inc. Publishers.
Bryson, G., Bell, M., & Lysaker, P. (1997). Affect recognition in schizophrenia: a function of global impairment or a specific cognitive deficit. Psychiatry Res, 71,105–113.
Buchanan, T. W., Tranel, D., & Adolphs, R. (2004). Anteromedial temporal lobe damage blocks startle modulation by fear and disgust. Behav Neurosci, 118, 429–437.
Buckholtz, J. W., Treadway, M. T., Cowen, R. L., Woodward, N. D., Benning, S. D., Li, R., Ansari, M. S., Baldwin, R. M., Schwartzman, A. N., Shelby, E. S., Smith, C. E., Cole, D., Kessler, R. M., & Zald, D. H. (2010). Mesolimbic dopamine reward system hypersensitivity in individuals with psychopathic traits. Nat Neurosci, 13, 419–421.
Cannon, W. B. (1929). Bodily changes in pain, hunger, fear and rage. New York: Appleton.
Colle, L. M., & Wise, R. A. (1988). Facilitory and inhibitory effects of nucleus accumbens amphetamine on feeding. In P. W. Kalivas & C. B. Nemeroff (Eds.), The mesocorticolimbic dopamine system (pp. 491–492). Annals of the New York Academy of Science, Vol 537.
Corr, P. J., & Kumari, V. (2013). Effects of d-amphetamine on emotion-potentiated startle in healthy humans: implications for psychopathy and antisocial behavior. Psychopharmacology, 225, 373–379.
Dara, C., Monetta, L., & Pell, M. D. (2008). Vocal emotion processing in Parkinson’s disease: reduced sensitivity to negative emotions. Brain Res, 1188, 100–111.
Davis, M., Falls, M., Campeau, S., & Kim, M. (1993). Fear potentiated startle: A neural and pharmacological analysis. Behav Brain Res, 58, 175–198.
Deans, E. (2011, May). Dopamine primer. How dopamine makes us human. Psychology Today. Retrieved from http://www.psychologytoday.com/blog/evolutionary-psychiatry/201105/dopamine-primer
Delaveau, P., Salgado-Pineda, P., Micallef-Roll, J., & Blin, O. (2007). Amygdala activation modulated by levodopa during emotional recognition processing in healthy volunteers: A double-blind, placebo-controlled study. J Clin Psychopharm, 27,692–697.
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, 29, 96–104.
Fridell, M., Hesse, M., Jaeger, M. M., & Kuhlhorn, E. (2008). Antisocial personality disorder as a predictor of criminal behaviour in a longitudinal study of a cohort of abusers of several classes of drugs: Relation to type of substance and type of crime. Addict Behav, 33, 799–811.
Funayama, E. S., Grillon, C., Davis, M., & Phelps, E. A. (2001). A double dissociation in the affective modulation of startle in humans: Effects of unilateral temporal lobectomy. J Cogn Neurosci, 13, 721–729.
Griffin, M. G., & Taylor, G. T. (1995). Norepinephrine modulation of social memory: Evidence for a time-dependent functional recovery of behavior. Behavioral Neuroscience, 109(3), 466–473.
Hariri, A. R., Mattay, V. S., Tessitore, A., Fera, F., Smith, W. S., & Weinberger, D. R. (2002). Dextroamphetamine modulates the response of the human amygdala. Neuropsychopharmacol, 27, 1036–1040.
Hohmann, G. W. (1966). Some effects of spinal cord lesions on experienced emotional feelings. Psychophysiology, 3, 143–156. James, W. (1890). Principles of psychology. New York: Holt.
Kiyatkin, E. A. (1995). Functional significance of mesolimbic dopamine. Neuroscience and Biobehavioral Reviews, 19(4), 573–598.
Kroner, S., Rosenkranz, J. A., Grace, A. A., & Barrionuevo, G. (2005). Dopamine modulates excitability of basolateral amygdala neurons in vitro. J Neurophysiol, 93, 1598–1610.
Kruk, A. L., & Pycock, C. J. (1991). Neurotransmitters and drugs. New York: Chapman and Hall.
Lee, T. H., Ellinwood Jr., E. H., & Nishita, J. K. (1988). Dopamine receptor sensitivity changes with chronic stimulants. In P. W. Kalivas & C. B. Nemeroff (Eds.), The mesocorticolimbic dopamine system (pp. 324–329). Annals of the New York Academy of Sciences, Vol 537.
Levenson, R. W., Ekman, P., & Friesen, W. V. (1990). Voluntary facial action generates emotion-specific autonomic system activity. Psychophysiology, 27, 363–384.
Mandal, M. K., Jain, A., Haque-Nizamie, S., et al. (1999). Generality and specificity of emotion–recognition deficit in schizophrenic patients with positive and negative symptoms. Psychiatry Res, 87, 39–46.
Miller, T. R., Levy, D. T., Cohen, M. A., Cox, K. L. C. (2006). Costs of alcohol and drug-involved crime. Prev Sci, 7, 333–342.
Missale, C., Nash, S. R., Robinson, S. W., Jaber, M., & Caron, M. G. (1998). Dopamine receptors: From structure to function. Physiol Rev, 78, 189–225.
Newton, P. M. (2009, April). What is dopamine? The neurotransmitter’s role in the brain and behavior. Psychology Today. Retrieved from http://www.psychologytoday.com/blog/mouse-man/200904/what-is-dopamine
Plutchik, R. (1994). The psychology and biology of emotion. New York: Harpercollins.
Post, R. M., Weiss, S. R. B., & Pert, A. (1988). Cocaine-induced behavioral sensitization and kindling: Implications for the emergence of psychopathology and seizures. In P. W. Kalivas & C. B. Nemeroff (Eds.), The mesocorticolimbic dopamine system (pp. 292–308). Annals of the New York Academy of Sciences, Vol 537. Psychology Today (1991-2013).
Dopamine. What is dopamine? Retrieved from http://www.psychologytoday.com/basics/dopamine
Salamone, J. D. (1996). The behavioral neurochemistry of motivation: Methodological and conceptual issues in studies of the dynamic activity of nucleus accumbens dopamine. Journal of Neuroscience Methods, 64(2), 137–149.
Salgado-Pineda, P., Delaveau, P., Blin, O., & Nieoullon, A. (2005). Dopaminergic contribution to the regulation of emotional perception. Clin Neuropharmacol, 28(5), 228-237.
Scatton, B., D’Angio, M., Driscoll, P. & Serrano, A. (1988). An in vivo voltammetric study of the response of mesocortical and mesoaccumbens dopaminergic neurons to environmental stimuli in strains of rats with differing levels of emotionality. In P. W. Kalivas & C. B. Nemerodd (Eds.), The mesocorticolimbic dopamine system (pp. 124–137) Annals of the New York Academy of Sciences.
Schachter, S. (1975). Cognition and peripheralist-centralist controversies in motivation and emotion. In M. S. Gazzaniga and C. Blakemore (Eds.), Handbook of psychobiology (pp. 529–564). New York: Academic Press.
Schachter, S., & Singer, J. (1962). Cognitive, social, and physiological determinants of emotional state. Psychological Review, 69, 379–399.
Schneider F, Gur RC, Gur RE, et al. (1995). Emotional processing in schizophrenia: neurobehavioral probes in relation to psychopathology. Schizophr Res, 17, 67–75.
Takahashi, H., Yahata, N., Koeda, M., Takano, A., Asai, K., Suhara, T., & Okubo, Y. (2005). Effects of dopaminergic and serotonergic manipulation on emotional processing: A pharmacological fMRI study. NeuroImage, 27, 991–1001.
Tassin, J. P., Herve, D., Blanc, G. & Glowinski, J. (1980). Differential effects of a two-minute open field session on dopamine utilization in the frontal cortices of BALB/C and C57 BL/6 mice. Neuroscience Letters, 17, 67–71.
Tennov, D. (1979). Love and limerence: The experience of being in love. New York: Stein and Day.
Whittaker, J. F., Deakin, J. F., & Tomenson, B. (2001). Face processing in schizophrenia: defining the deficit. Psychol Med, 31,499–507.
Wise, R. A. (1988). Psychomotor stimulant properties of addictive drugs. In Kalivas, P. W. & C. B. Nemeroff (Eds.), The mesocorticolimbic dopamine system (pp. 228–234). Annals of the New York Academy of Sciences, Vol 537.