Pleasure center

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Pleasure center is the general term used for the brain regions involved in pleasure. Discoveries made in the 1950s initially suggested that rodents could not stop electrically stimulating parts of their brain, mainly the nucleus accumbens, which was theorized to produce great pleasure.[1] Further investigations revealed that the septum pellucidium and the hypothalamus can also be targets for self-stimulation.[2] More recent research has shown that the so-called pleasure electrodes lead only a form of wanting or motivation to obtain the stimulation, rather than pleasure.[3] The weight of evidence suggests that human pleasure reactions occur across a distributed system of brain regions, of which important nodes include subcortical regions (such as the nucleus accumbens and ventral pallidum) and cortical regions (orbitofrontal cortex and anterior cingulate cortex).[4]

Rodent experiments[edit]

The pleasure center was discovered in the 1950s by two brain researchers named James Olds and Peter Milner who were investigating whether rats might be made uncomfortable by electrical stimulation of certain areas of their brain, particularly the limbic system.[5] In the experiment, an electric current was given to rats if they entered a certain corner of a cage, with the hypothesis that they would stay away from that corner if the effect was uncomfortable. Instead, they came back quickly after the first stimulation and even more quickly after the second. In later experiments, they allowed the rats to press the stimulation lever themselves, to the effect that they would press it as much as seven-hundred times per hour. This region soon came to be known as the "pleasure center".

Rats in Skinner boxes with metal electrodes implanted into their nucleus accumbens will repeatedly press a lever which activates this region, and will do so in preference over food and water, eventually dying from exhaustion. In rodent physiology, scientists reason that the medial forebrain bundle is the pleasure center of rats. If a rat is given the choice between stimulating the forebrain or eating, it will choose stimulation to the point of exhaustion.[6]

Human experiments[edit]

Dr. José Manuel Rodriguez Delgado implanted electrodes in the brains of 25 people.[7]

  • 1972: A 24-year-old man with temporal lobe epilepsy, identified as patient "B-19". "He was permitted to wear the device for 3 hours at a time: on one occasion he stimulated his septal region 1,200 times, on another occasion 1,500 times, and on a third occasion 900 times. He protested each time the unit was taken from him, pleading to self-stimulate just a few more times... " [9][10][11]
  • 1986: A 48-year-old woman with chronic pain. "the patient self-stimulated throughout the day, neglecting personal hygiene and family commitments."[12]

Brain regions[edit]

Nucleus accumbens[edit]

The nucleus accumbens (NAcc), part of the limbic system, plays a role in sexual arousal and the "high" derived from certain recreational drugs. These responses are heavily modulated by dopaminergic projections from the limbic system. The NAcc is a recognized reward center, and activation of the pathway from the ventral tegmental area to the Nacc is believed to be rewarding, which is why it is sometimes referred to as the hedonic highway.[13] The MFB also contains serotonergic and noradrenergic fibers.

Brain interactions with the nucleus accumbens[edit]

The nucleus accumbens (NAcc) is a unique component of the brain, since it cannot elicit reward and learning responses without letting the brain inject dopamine into it or without letting the brain process the stimuli received. One model known as the triadic model of neurobiology has been used to attempt to explain what initiates motivation. The triadic model is based on three components of the brain that need to interact with each other constantly:

  • the amygdala
  • the nucleus accumbens
  • the ventral medial prefrontal cortex

Current research shows that the NAcc creates a strong reward system, while the amygdala creates a harm avoidance system for an action and the ventral medial prefrontal cortex supervises that particular action. With these components working in unison, the brain is able to create what we know as motivation.[14] Certain brain receptors also have the ability to alter the behavior of the pleasure center. Receptors in the NAcc have to open and close to respond to dopamine and serotonin. But there are other receptors that may open and close to other substances and these may inhibit or enhance the behavior of the NAcc. For example, group II metabotropic glutamate receptors (mGluR2 and mGluR3) may play a role in the pathology of cocaine addiction.[15] It was observed that the mGluR2 and R3 receptors decrease the body’s need for cocaine. So while the NAcc might allow the body to become dependent, these receptors may also work with the NAcc to keep the dependency at an attenuated level.

Prefrontal cortex[edit]

The limbic system is closely connected to the prefrontal cortex. Some scientists contend that this connection is related to the pleasure obtained from solving problems[citation needed]. In a now-obsolete practice to cure severe emotional disorders, this connection was sometimes surgically severed, a procedure of psychosurgery, called a prefrontal lobotomy (a misnomer). Patients who underwent this procedure often became passive and lacked all motivation.

Medial Forebrain Bundle[edit]

It is commonly accepted that the MFB is a part of the reward system, involved in the integration of reward and pleasure.[16]

Electrical stimulation of the medial forebrain bundle is believed to cause sensations of pleasure. This hypothesis is based upon intracranial self-stimulation (ICSS) studies. Animals will work for MFB ICSS, and humans report that MFB ICSS is intensely pleasurable.[17] It is possible that the medial forebrain bundle carries some of the input from the ventral tegmental area (VTA) to the nucleus accumbens (NAcc or Acb).

Actions and rewards[edit]

The NAcc is linked to the rewarding of human behaviors. But human behaviors or actions can only be rewarded if there are cues to remind us of what a particular action felt like.[18] The human brain and the cluster of Neurons (NAcc) partner together to provide these clues by releasing neurotransmitters. The two main neurotransmitters that are released into the NAcc upon certain stimulation are dopamine and serotonin. Serotonin is known as the neurotransmitter that gives the body the impression of satisfaction and hence the body no longer desires the stimulant that was provided initially. Conversely, dopamine is the neurotransmitter that increases the desire for that stimulant.[19] With these neurotransmitters being released into the NAcc it becomes clear that certain behaviors are driven by a reward or anticipation of a reward. The body remembers the pleasurable feeling of the reward and that particular action or behavior can be committed to memory. It is good to keep in mind that the brain's reward system is not only responsive to neurotransmitters. The brain can also take social interactions and use these to create a reward system based on the pleasure of a social interaction.[20]


Sex is an act that can be committed to memory as a pleasurable or disturbing act, depending on the neurotransmitter released. Dopamine is actually involved in sexual motivation and reward as discovered in male rats.[21] Female rodents have not been extensively tested but a transcription factor named delta FosB (ΔFosB) has been shown to increase the sexual efficiency of Syrian female hamsters when injected into the NAcc.[22]


Further information: ΔFosB

Addiction has been linked to structural changes in the brain, especially within the pleasure center (NAcc). The structural changes in the nucleus accumbens and behavioral changes that arise from addiction are primarily induced by overexpression of ΔFosB in the NAcc.


The above information is based on pioneering research and experimental design. This research has useful benefits for the therapy and rehabilitation. The test subjects range from mice to rats to primates. Rodents are preferred because of their size and easy handling, but are mostly chosen because the effects of the NAcc seem to take effect much more quickly than they do in primates. In other words they learn, become addicted or acquire a reward system at a faster rate than humans.


Neurologists, biologists and psychologists continue to be interested in the effects of the NAcc. Substance abuse is a common point of research. Stimulants, such as cocaine, are the choice of drug used in trying to determine the reward and addiction response of the NAcc.[23] Cocaine not only has adverse consequences for the NAcc but it has adverse consequences for other neurotransmitters and other receptors.


Memory and attention are also areas that are researched in relation to the NAcc. It is currently understood that the organic solvent toluene interacts with the dopamine and NMDA receptors and causes memory impairment.[24] This is pertinent information because toluene is used in many commercial products such as paint removers, rubber, ink and leather.


The causes of stress and the body’s response to stress are a well known and researched subject. The NAcc may also play a role in initiating and maintaining stress.[25] Again, this is probably determined by the amount of neurotransmitters and their receptors that can interact with dopamine and serotonin. Trying to reduce the activity of the NAcc during a stressful scenario has shown a decrease in the dependence of cigarettes[26] and may have the same effects on other substances that individuals have become dependent on.

Video games[edit]

Video games may present a form of addiction for some. There is research that is making strides in trying to determine the similarities between the pathway of regular substance abuse in relation to the NAcc and in the pathway of video game addiction. The activation of nucleus accumbens under gaming cue suggests that it may reactivate the emotional memory of previous gaming and enhance the motivation for game-seeking behavior.[27]

Future research[edit]

There are steps being made to get a greater understanding of the NAcc and its interactions with other components of the brain. Brain imaging has seen the most advances in this area. fMRI has been used to show what regions of the brain are also involved in the reward, motivation and addiction pathways. Brain imaging techniques have been used to decipher the mental demeanor of stock traders as they make daily trades. Brain imaging showed an interesting trend. The participants who were shown a picture of a smiling face were more likely to invest in risky stocks than those who were shown a picture of a serious face. Brain imaging showed that the NAcc was activated after the smiley face was shown and before the risky stock was picked.[28]

Depression has adverse effects on the psychological activities of the brain and the physical activities of the human body. It could be that the NAcc can be regulated to treat depression by a means other than medication. Music has been used to stimulate the NAcc of depressed patients, showing a positive correlation between the stimulation of the NAcc and a patient’s favorite song.[29]

See also[edit]


  1. ^ Olds, James (1956) Pleasure centers in the brain. Scientific American. 105-116.
  2. ^ Routtenberg, Aryeh (1978) The reward system of the brain. Scientific American. 154-164.
  3. ^ Berridge, K.C., Kringelbach, M.L. (2008) Affective neuroscience of pleasure: Reward in humans and other animals. Psychopharmacology 199, 457-80.
  4. ^ Kringelbach, M.L (2009). The pleasure center: Trust Your Animal Instincts. Oxford University Press. ISBN 978-0-19-532285-9. 
  5. ^ Liebowitz, Michael, R. (1983). The Chemistry of Love. Boston: Little, Brown, & Co.
  6. ^ Whitters, W.L. & Jones-Whitter, P. (1980). Human Sexuality - A Biological Perspective. New York: Van Nostrand.
  7. ^ "The Forgotten Era of Brain Chips"
  8. ^ Heath, R.G. (December 1, 1963) Electrical self-stimulation of the brain in man. American Journal of Psychiatry 120: 571-577.
  9. ^
  10. ^
  11. ^ Moan, C.E., & Heath, R.G. (1972) Septal stimulation for the initiation of heterosexual activity in a homosexual male. Journal of Behavior Therapy and Experimental Psychiatry 3: 23-30.
  12. ^
  13. ^ The Owner's Manual for the Brain: Everyday Applications from Mind-Brain Research, 3rd ed. 2006. Austin: Bard Press. ISBN 1-885167-64-4
  14. ^ Ernst, M (2009) Triadic model of the neurobiology of motivated behavior in adolescence
  15. ^ Megan M Moran. Cystine/Glutamate Exchange Regulates Metabotropic Glutamate Receptor Presynaptic Inhibition of Excitatory Transmission and Vulnerability to Cocaine Seeking. Journal of Neuroscience 7/6/2005, Vol. 25 Issue 27, p6389-6393 5p; 4 graphs 02706474
  16. ^ Hernandez G, Hamdani S, Rajabi H et al. (August 2006). "Prolonged rewarding stimulation of the rat medial forebrain bundle: neurochemical and behavioral consequences". Behav. Neurosci. 120 (4): 888–904. doi:10.1037/0735-7044.120.4.888. PMID 16893295. 
  17. ^
  18. ^
  19. ^
  21. ^ 2001. Dopamine and male sexual function. Giuliano F, Allard J.
  22. ^ Hedges VLDelta FosB overexpression in the nucleus accumbens enhances sexual reward in female Syrian hamsters (vol 8, pg 442, 2009)
  23. ^ Sun, Wei-Lun Cocaine effects on dopamine and NMDA receptors interactions in the striatum of Fischer rats
  24. ^ Lo, Pi-Shih (2009) Acute neurobehavioral effects of toluene: Involvement of dopamine and NMDA receptors
  25. ^ The beta-Endorphin Role in Stress-Related Psychiatric Disorders
  26. ^ An acute psychosocial stress enhances the neural response to smoking cues Alain Daghe. Vol 1293. 1 October 2009, Pages 40-48 Stress, Coping, and Disease
  27. ^ Brain activities associated with gaming urge of online gaming addiction Chih-Hung Ko.(2009)
  28. ^ Happy traders take more risks. Peter Aldhous. New Scientist 4/4/2009, Vol. 201 Issue 2702, p9-9 1p 02624079
  29. ^ EA Osuch. NEUROREPORT 20 (13): 1204-1208 AUG 26 2009. Brain Activation to Favorite Music in Healthy Controls and Depressed Patients

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