Joy is both the physiological experience of warmth and satisfaction and the cognitive assessment that this is the way things should be. Joy, happiness, pleasure, is its own incentive; it is what makes survival and propagation of the species worthwhile.
Some of the earliest research on happiness was serendipitous. In the 1950s James Olds and Peter Miler, hoping to influence learning, placed an electrode into the hypothalamus of a rat. When the rat pressed a bar connected to the electrode, the hypothalamus was stimulated. The researchers concluded that the rat perceived this sensation as pleasurable because it proceeded to press the bar up to 4,000 times an hour, and would allow itself to starve rather than stop. They had hit upon the pleasure center of the brain. Since then, research with humans has shown that the hypothalamus is just one of several pleasure centers of the brain, among them the septum and the nucleus accumbens.
Neurotransmitters and endorphins play an important role in the perception of pleasure. But dopamine is a key factor, and the one currently getting the most attention. Each of the pleasure centers uses dopamine as a transmitter. If a rat is trained to push a lever for internal stimulation to a pleasure center and is then given a drug such as pimozide or haloperidol that blocks the action of dopamine, the rat will stop pushing the lever. Pleasure is often muted in people who are taking conventional antipsychotic drugs, which block the dopamine receptors. The drugs are used to stop hallucinations and delusions, but often produce a state of joylessness and a lack of motivation and drive. As this can complicate treatment, newer drugs that have less of this effect are being developed to treat psychoses. Meanwhile, drugs such as cocaine and amphetamines work in the brain by increasing dopamine levels. But if dopamine, or any of its artificial substitutes reaches levels that are too high, hypomania or even mania can result.
It is hard to imagine a disorder arising from too much happiness, but there are several that can result from not having enough happiness or enough internal reinforcement and feelings of pleasure. Reward deficiency syndrome, a concept coined by Ken Blum at the University of Texas, is helpful in understanding the complexities of addiction and compulsive behavior. This idea states that a lack of internal rewards leads a person to self-medicate with substances or with behavior thai is rewarding. We see evidence for this in the statistics for conduct disorder and ADD; children who have either of these illnesses are 5 times more likely to be addicted to drugs or alcohol as adults compared with the general population.
While different neurotransmitter systems cascade upon one another in the reward mechanism of the human brain, perhaps the most important interaction is that of dopamine in the nucleus accumbens, a group of neurons that have a special relationship to reward and motivation. It is located just beneath the front of the striatum, a part of the basal ganglia which is involved in movement and cognition. If the nucleus accumbens is lesioned in lab rats that normally push a lever to receive addictive drugs such as cocaine, the rats will stop pushing.
Recent research at the University of Cagliari has shown that within the nucleus accumbens there is a further division of function. In a study that supports conclusions about the addictive effect of nicotine, were injected with nicotine directly into the brain and scientists observed corresponding increases of dopamine and activity in the nucleus accumbens. This area of the brain behaves similarly when cocaine, amphetamine, or morphine is administered. An important finding in this study is that a difference was identified between the action of the outer shell of the nucleus accumbens and its inner core. The outer shell seems to be most involved in emotion, motivation, and addiction. This area has direct connections to the limbic system and is part of the extended amygdala, which serves as a link between the brain and the forebrain.
This area is important for learning, in part because it tags information with a signal of intensity that tells the rest of the brain to pay attention. Stimulating this area with an electrode helps rats to learn more quickly and use more extensive areas of the cortex during learning. The extended amygdala’s emotional coloring of learning affects our notions about the rewards and dangers of different stimuli.
There is still much to be learned from research on addiction. A research group at Yale University is examining the different roles that dopamine receptor subtypes play in creating and maintaining addiction. Understanding the processes of addiction and motivation more thoroughly could possibly remove the stigma and improve treatment for disorders ranging from alcoholism and drug abuse to gambling and sex and food addictions.
One of the most intriguing emotions in the spectrum of joy is love. While most of us wax poetic about it, some researchers are breaking it down in typically rigorous laboratory fashion. According to Helen Fisher, an anthropology professor at Rutgers University, there are three distinctly different physiological and emotional categories of lovelust, attraction, and attachment, and biologically, at least, they all relate to the ancient drive to mate. Fisher says that each behavior evolved with a different purpose. Lust evolved to get you out looking; attraction evolved to make you focus and expend your energy on one specific individual; and attachment evolved so you would stay with that individual and raise offspring once mating was accomplished.
Using MRI scans that show chemical activity in the brain, Fisher has found that lust is associated primarily with estrogen and androgens. Attraction, however, is associated with elation and a craving for emotional union, which may be linked to the monoamines such as seratonin. The neurotransmitters associated with long-term attachment, a behavior evidenced by close body contact, separation anxiety, and a sense of calm, security, and peace with a to find. Fisher hopes that the results of her ongoing work will show that the stages of love are based at least as much in brain chemistry and physiology as they are in psychology, further evidence backing up the thesis that emotion is not one system in the brain but multiple systems that tie together workings of the brain and the body. We all know this is true: early in our relationships with our current lovers or spouses, our hearts raced when we suddenly heard their voices on the phone; we had butterflies in our stomachs when we prepared to meet them.
These kinds of physical sensations are linked to increased quantities of neurotransmitters such as dopamine, serotonin, and norepineph rifle in the brain’s pleasure centers, as well as other chemicals such as oxytocin, endorphins, and phenylethylamine (PEA), known as the “love drug.” These brain chemicals are also the ones long associated with various states of euphoria and in particular with the ecstasy caused by drugs such as cocaine and amphetamines, as well as with the high that long-distance runners report experiencing. The chemical compounds in chocolate act like nicotine, causing the release of dopamine in the pleasure centers.
Of course, not all joy is brought on by physiological stimuli. We are happy when we receive praise, find a dollar, or finish a puzzle. When ever I show a picture of my basset hounds to someone, the person inevitably smiles. These stimuli start the pleasure ball rolling by eliciting a small squirt of dopamine, serotonin, and oxytocin in the pleasure centers.
One of the most joyful of emotions is laughter, but the neurochemistry of it is hard to explain. We laugh when something strikes us as funny. But we also laugh when we are nervous and sometimes just because someone else is laughing. Laughter derives from the primary emotion of joy, but it’s a bit confounding because of the many and varied circumstances that trigger it.
Robert Provine, a behavioral neurobiologist at the University of Maryland, studied students on college campuses to find out exactly what made people laugh; 1,200 “laugh episodes” later, he was convinced that most laughter has little to do with jokes or funny stories. Clearly, social context is important; people laugh as noted when they’re nervous as well as when they are amused, and they may laugh cynically when disappointed. While laughter is evoked by a punch line, indicating that the brain’s conscious, cognitive regions must decide that the circumstances are right for laughter, most people cannot will themselves to laugh on command or to suppress an unwanted case of the giggles. Laughter arises from our conscious minds and from a primitive, precognitive part of our brains, something that’s very deep in our animal nature.
Recent study also indicates that laughter may be primarily a function of the left hemisphere. In 1998 doctors at the University of California of Los Angeles reported that they were able to make a sixteen-year-old girl laugh by stimulating a tiny region in the left frontal lobe, the supplemental motor cortex. They were testing her to try to find the source of her epileptic seizures. When they stimulated that particular region with an electric current, the girl burst out laughing. She was asked to perform various tasks, such as naming objects, reading, counting, and extending her forearms, but regardless of the activity, she consistently laughed when that area was stimulated. Even more interesting was the fact that although the girl’s laughter was being triggered electrically, each time she laughed she had a different explanation for it, attributing it to whatever object was in front of her or whatever action she was engaged in at the time. She saw a picture of a horse as hilarious, giggled over a book she was reading, and once told the researchers, “You guys are just so funny.”
Provine says that, in part, laughter functions as a kind of social signal, just like a smile or a scowl. Indeed, studies have shown that people are thirty times more likely to laugh in social settings than when they are alone. Even nitrous oxide loses much of its potency if taken in solitude. Laughter occurs when people are comfortable with one another, and the more laughter, the more bonding within the group, lending credence to the old saw that laughter is “contagious.” If there is a feedback loop of bonding-laughter-more bonding, it may explain one of the most bizarre incidents of contagious laughter ever recorded: in 1962, an epidemic of laughter among schoolgirls in Tanganyika lasted for six months and forced officials to close schools to break up the group and end the marathon.