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The Dopamine High: From Social Networking to Survival

By Victoria Saadat

Published on August 21, 2012

Logging onto Facebook or any other social networking site immediately introduces a barrage of status updates from friends reporting where they are, what they are eating, and what beverage they are purchasing at the coffee shop. While many ask why people incessantly report their perfunctory daily activities, a report from scientists at Harvard University demonstrates that our brain's dopamine reward pathway, in fact, rewards us for talking about ourselves. This reward pathway is responsible for many other essential mind-body functions that have enhanced the survival of the human species [1]. At the center of this intricate system of signals and functions is the neurotransmitter molecule, dopamine.

Courtesy of David Darling/Encyclopedia of Science

Figure 1: Neurotransmitters are released from synaptic vesicles of the presynaptic neuron and bind to receptors on the postsynaptic neuron, thereby triggering an impulse through the second neuron.

Neurotransmitters: the Brain's Chemical Messengers

Neurotransmitters are the brain's chemical messengers, responsible for regulating the plethora of physical and emotional processes in our bodies. Emotional states and pain response, for example, are just two of the essential roles of these molecules [2]. These molecules carry information through their biochemical structures and function at the synapse, the site of neuron-to-neuron connections. Neurons are specialized nerve cells that send, receive, process, and transmit information by regulating the amount and frequency of release of neurotransmitters. Information enters the neuron via the dendrites from adjacent neurons, passes through the cell body, and is conducted down the axon until it reaches the terminal buttons at the end of the neuron [3]. These bulb-shaped terminal buttons are responsible for sending the signal to other neurons. At a terminal end, neurotransmitters are released from vesicles inside the cell into the synaptic cleft, a region between neighboring neurons, and then travel to receptor sites on the receiving neuron (see Figure 1) [4].

The Neurotransmitter Dopamine

Dopamine, in particular, has been studied in the fields of human psychology and behavior. A small-molecule neurotransmitter, dopamine is characterized by biochemists as a biogenic amine, a type of signaling amine synthesized by animals [4]. Dopamine's excitatory effects have been uncovered by studies investigating the molecule's many roles in mental health and homeostasis. Responsible for motivation, drive, and interest, dopamine has been associated with states such as exercising, being in love, and listening to music [2]. A lack of dopamine depletes our concentration, energy, and initiative spirit. Even with this in mind, any increase or decrease in the homeostatic levels of dopamine is a cause for concern and potentially a basis for disease [3]. For example, as dopamine is often correlated with coordinated muscle movement, a fall in its concentration is a contributing factor in the muscular rigidity characteristic of Parkinson's disease. An increase of dopamine concentration beyond the normal level is a causative factor in the progression of schizophrenia [4].

Courtesy of National Institute of Drug Abuse (NIDA) of the National Institutes of Health (NIH)

Figure 2: The nucleus accumbens (NAcc) and ventral tegmental area (VTA) are involved in the mesolimbic dopamine reward pathway.

While the mysteries of the brain, including the roles of dopamine, still abound in the neurosciences, it is known that this neurotransmitter is an integral part of a neural highway called the mesolimbic dopamine reward pathway. This circuit, which involves regions of the brain such as the nucleus accumbens (NAcc) and ventral tegmental area (VTA) (see Figure 2), is attributed to most feelings of pleasure [5]. Rushes of both dopamine and serotonin are associated with the experiences of eating, drinking, and sleeping, causing "primary reinforcement," a trigger system that teaches us to continue these pleasure-inducing behaviors [4]. Why is the dopamine reward pathway so vital to our survival as a species? Well, imagine living without eating or sleeping for one week.

Dopamine and the Rewards of Self-Disclosure

A study conducted by researchers at Harvard University tested the theory that people more highly value their own experiences over those of others, and that self-disclosure, or the act of talking about oneself, positively triggers dopamine reward pathways. Functional magnetic resonance imaging (fMRI) was used to visualize which parts of the brain were engaged during self-disclosure. The researchers determined whether subjects would prefer reporting their own experiences to receiving a small monetary reward. When participants were asked to choose between expressing their own opinions, judging the opinions of others, or answering factual questions, with each option having an equal monetary reward, participants preferred self-disclosure over opinions of others 69% of the time and over factual questions 66% of the time. When the three options were associated with differing monetary awards, participants would choose self-disclosure over the other two options even when self-disclosure resulted in a smaller payoff, resulting in an average loss of 17% in monetary rewards. Imaging studies strengthened this conclusion, revealing increased activity in the NAcc and VTA regions of the mesolimbic dopamine circuit during self-disclosure in comparison with non-self discussions [6]. These findings strongly suggest that the human tendency to share information about personal experiences with others is intimately connected with the positive reward triggers in the dopamine reward pathway. Furthermore, these results confirm the psychological tie-in of social networks to human behavior [7]. An extremely psychologically intuitive business model, social networks take cues from human psychology and sell that service to advertisers.

Courtesy of National Institute of Drug Abuse (NIDA) of the National Institutes of Health (NIH)

Figure 3: Dopamine released into the synapse is returned to the presynaptic neuron, a process known as reuptake.

When Dopamine Activity Goes Awry

Although dopamine reward pathways abound as part of the body's regulatory and sensory systems, disruptions to these pathways can result in diseases. For example, attention deficit hyperactivity disorder (ADHD), which affects 9.5% of children of ages 4-17 in the United States, can result from irregular dopamine activity [8]. In normal neuronal function, neurotransmitters are released from the presynaptic neuron when an action potential reaches the terminal button containing the neurotransmitter-filled vesicles. Thereafter, these chemicals enter the synaptic space, binding to receptors on the postsynaptic neuron and triggering a chemical signal in that neuron. The neurotransmitters that are not absorbed by the postsynaptic neuron are typically returned to the presynaptic vesicles, a process known as reuptake (see Figure 3), and stored again until the next impulse triggers their release again. However, at synapses of those affected by ADHD, the neuronal signal is not passed efficiently from the presynaptic neuron to the postsynaptic neuron through dopamine. Scientists have determined that multiple components of the transmission process may be affected in patients with ADHD: insufficient amounts of dopamine may be released by presynaptic vesicles, or not enough of the neurotransmitter is absorbed by the postsynaptic neuron [9]. In fact, patients with ADHD have fewer dopamine transporters in the brain, resulting in less dopamine release into the synapse [10]. Disruptions in the signal transmission process result in the need for medical treatments to target the synapse. In cases in which a greater quantity of neurotransmitter needs to be released, the stimulants Ritalin and Adderall are often prescribed to increase the amount of dopamine released after each action potential by preventing reuptake of dopamine into the presynaptic neuron, thereby extending its action on the postsynaptic neuron's receptors [11].

Conclusion

The dopamine pathway clearly is associated with a range of functions, from driving us to perform necessary processes such as eating and sleeping to promoting the act of self-disclosure that is associated with social networks. Due to its role in normal human behavior, any small disruption in the cycle of dopamine release and recognition can cause profound damage to the body's ability to function normally. Deficiencies in dopamine release and recognition lead to the symptoms of ADHD, while proper functioning of the neurotransmitter drives some of our most basic evolutionary drives—the drive to eat, sleep, and be happy.

Works Cited

1. M. Peck. "Facebook Loves It When You Talk About Yourself – and so Does Your Brain." IEEE Spectrum: Inside Technology. May 10, 2012. Available: http://spectrum.ieee.org/tech-talk/biomedical/diagnostics/facebook-loves-it-when-you-talk-about-yourself-and-so-does-your-brain.

2. Integrative Psychiatry. "The Four Major Neurotransmitters." Available: http://www.integrativepsychiatry.net/neurotransmitter.html.

3. AllPsych and Heffner Media Group, Inc. "Neurotransmitters." Available: http://allpsych.com/psychology101/neurotransmitters.html.

4. Lundbeck Institute. "Neurological Control: Neurotransmitters." December 20, 2011. Available: http://www.brainexplorer.org/neurological_control/Neurological_Neurotransmitters.shtml.

5. C. Bailey. (2005.) "Neuronal Pathways Involved in Reward and Addiction." E-journal of the British Pharmacological Society 3(3).

6. D. Tamir and J. Mitchell. (2012.) "Disclosing information about the self is intrinsically rewarding." Proceedings of the National Academy of Sciences 109(21): 8038-43.

7. R. Hotz. (2012.) "Science Reveals Why We Brag So Much." Health & Wellness. Available: http://online.wsj.com/article/SB10001424052702304451104577390392329291890.html.

8. Centers for Disease Control and Prevention. (2010.) "Increasing Prevalence of Parent-Reported Attention-Deficit/Hyperactivity Disorder Among Children --- United States, 2003 and 2007." Morbidity and Mortality Weekly Report (MMWR) 59(44): 1439-43. Available: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5944a3.htm?s_cid=mm5944a3_w.

9. N.D. Volkow, G-J. Wang, S.H. Kollins, et al. (2009.) "Evaluating Dopamine Reward Pathway in ADHD." Journal of the American Medical Association 302(10): 1084-91.

10. N.D. Volkow, G-J. Wang, J. Newcorn, et al. (2007.) "Brain dopamine transporter levels in treatment and drug naïve adults with ADHD." Neuroimage 34(3): 1182-90.

11. D. Sulzer, M.S. Sonders, N.W. Poulsen, et al. (2005.) "Mechanisms of neurotransmitter release by amphetamines. A review." Progress in Neurobiology 75: 406-33.

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