Connect the Concepts: Gambling and the Brain
Skinner (1953) stated, “If the gambling establishment cannot persuade a patron to turn over money with no return, it may achieve the same effect by returning part of the patron’s money on a variable-ratio schedule” (p. 397).
Skinner uses gambling as an example of the power of the variable-ratio reinforcement schedule for maintaining behavior even during long periods without any reinforcement. In fact, Skinner was so confident in his knowledge of gambling addiction that he even claimed he could turn a pigeon into a pathological gambler (“Skinner’s Utopia,” 1971). It is indeed true that variable-ratio schedules keep behavior quite persistent—just imagine the frequency of a child’s tantrums if a parent gives in even once to the behavior. The occasional reward makes it almost impossible to stop the behavior.
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Recent research in rats has failed to support Skinner’s idea that training on variable-ratio schedules alone causes pathological gambling (Laskowski et al., 2019). However, other research suggests that gambling does seem to work on the brain in the same way as most addictive drugs, and so there may be some combination of brain chemistry and reinforcement schedule that could lead to problem gambling (Figure 6.14). Specifically, modern research shows the connection between gambling and the activation of the reward centers of the brain that use the neurotransmitter (brain chemical) dopamine (Murch & Clark, 2016). Interestingly, gamblers don’t even have to win to experience the “rush” of dopamine in the brain. “Near misses,” or almost winning but not actually winning, also have been shown to increase activity in the ventral striatum and other brain reward centers that use dopamine (Chase & Clark, 2010). These brain effects are almost identical to those produced by addictive drugs like cocaine and heroin (Murch & Clark, 2016). Based on the neuroscientific evidence showing these similarities, the DSM-5 now considers gambling an addiction, while earlier versions of the DSM classified gambling as an impulse control disorder.
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In addition to dopamine, gambling also appears to involve other neurotransmitters, including norepinephrine and serotonin (Potenza, 2013). Norepinephrine is secreted when a person feels stress, arousal, or thrill. It may be that pathological gamblers use gambling to increase their levels of this neurotransmitter. Deficiencies in serotonin might also contribute to compulsive behavior, including a gambling addiction (Potenza, 2013).
It may be that pathological gamblers’ brains are different than those of other people, and perhaps this difference may somehow have led to their gambling addiction, as these studies seem to suggest. However, it is very difficult to ascertain the cause because it is impossible to conduct a true experiment (it would be unethical to try to turn randomly assigned participants into problem gamblers). Therefore, it may be that causation actually moves in the opposite direction—perhaps the act of gambling somehow changes neurotransmitter levels in some gamblers’ brains. It also is possible that some overlooked factor, or confounding variable, played a role in both the gambling addiction and the differences in brain chemistry.
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