Psychologists have identified that the pleasure circuit in the brain is completely different than researchers had previously thought. Furthermore, their discoveries could completely shape the study of mental illness and a new science of happiness.
Most work on pleasure in the past three decades has been based on that of three researchers. In the 1950s, James Olds and Peter Millner read about research in which scientists had applied electrodes to the heads of rats. When an area of the brain was stimulated, animals would actively avoid recreating the action that had prompted the shock. When searching for this area of the brain, Olds and Millner attempted to recreate the experiment. Instead, they shocked another area of the brain. They found that mice would repeat the same action over and over again in order to receive the same stimulation. When mice were given the opportunity to give themselves a jolt, they did – sometimes over 1,000 times an hour.
Robert Heath built upon this research at around the same time period. His controversial experiments involved surgically implanting electrodes on the brains of patients institutionalized for severe neurological and mental disorders, like schizophrenia, epilepsy, and depression. He hoped that, by stimulating areas of the brain, he could cure their diseases.
These experiments helped to define an area of the brain known as the "pleasure center," an area that seemed to explain the biological underpinnings of pleasure – a sensation that is central to life, as it helps facilitate eating, sex, and other actions that perpetuate life. The idea remained steadfast – at least in popular culture – for decades.
But the problem, say psychiatrist and author Morten L. Kringelbach, and neuroscientist and psychologist Kent Berridge in the Scientific American, is that Heath never did cure these patients of their neurological and mental conditions. In fact, it has not led to any breakthroughs in mental illness whatsoever. Moreover, say Kringelbach and Berridge, the regions that researchers called the seat of pleasure, and the chemicals that they were activating, did not activate pleasure at all.
They activated desire.
Xiaoxi Zhuang from the University of Chicago conducted experiments that confirmed Kringelbach's and Berridge's hypothesis. Zhuang engineered two different sets of mice, one with too much dopamine and the other with none. Dopamine was chosen because the regions activated by Olds, Millner, and Heath were activated by neurotransmitter dopamine. Zhuang found that, while the rats with no dopamine were not going to seek out food, they enjoyed chocolate just as much as healthy rats. Meanwhile, those with increased dopamine also ate chocolate as much as healthy rats and even sought out treats more quickly, but their faces did not reflect pleasure. Their faces reflected disgust.
The same seems to be true in humans as well – and seems to be extremely pertinent to the study of addiction. Abused drugs bring a flood of dopamine, inducing cravings years after the drug no longer creates pleasure.
In addition to dopamine, two sections of the brain are responsible for creating pleasure: one is a sub-region of the nucleus accumbus called the medial shell; the other is the ventral palladium, which receives most of its directions from the nucleus accumbus. When stimulated, they make enjoyable things even more pleasurable. When one section was damaged, pleasure still existed, even if euphoria was harder to come by – for the most part. One patient whose ventral palladium was damaged reported feeling hopelessness and depression on a near-constant basis.
Researchers also found, with neuroimaging, a small area in the orbitofrontal cortex. When eating something tasty, like a brownie, the area lights up. But as you continue eating from the tray of brownies, the area starts to shut down until brownies are no longer enjoyable.
Morten L. Kringelbach and Kent Berridge are the authors of The Pleasure Center.