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Gambling as Behavioral Mirror of Action Potentials and Voltage-Gated Channels

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Gambling as Behavioral Mirror of Action Potentials and Voltage-Gated Channels


Human behavior and physiological function is built on the premise of action potentials and their proper functioning. In order for any behavior, active thought, movement, emotional reaction, or a host of other human acts to occur, an action potential must be fired along an axon, so as to facilitate, direct, and function in communication between various neuronal somas. In order for a behavior to occur, this communication must proceed among many neurons, so as to activate the areas of the brain and body, and overall nervous system that are necessary and responsible for physical or mental behavior. Action potentials are only fired when a certain threshold is reached at the voltage gated channels between which action potentials and neurotransmitters travel. For the fulfillment of this threshold, a certain voltage must be reached—even a minutely lesser voltage than threshold will not suffice to create and fire the action potential. Similarly, in addictive, psychoactive substance use disorders, particularly pathological gambling, a behavior must be repeated to a particular arbitrary frequency or intensity, before consequences are initiated or established.


Gambling and other addictive behaviors have long been thought of as having cognitive, behavioral components contributing to their execution, in addition to strong heritability and more physiological components. Behavioral aspects of the tendency toward addictive behaviors in gambling have been explained in part by the somatic marker theory of decision making. This theory was originally applied to alcoholism and addictive behaviors in substance use (Verdejo-Garcìa & Bechara, 2009). The somatic marker theory suggests that somatic markers—defined as “emotions and feelings that have been connected by learning to anticipated future outcomes of certain scenarios” (Verdejo-Garcìa & Bechara, 2009)—are internalized, such that these feelings and emotions are generated in the I-function of a person, and encourage the person to perform a behavior so as to achieve the expected, learned outcome or reward (Dretsch & Tipples, 2008).


This behavioral model is applied to gambling, as the pathological gambling patient population have learned expectations of situational outcomes that are summoned and triggered by encounters with cues to these behavioral stimuli (Verdejo-Garcìa & Bechara, 2009). Pathological gambling is defined by a series of criteria, outlined in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders, including constant gambling in which life assets are sacrificed and financial situation is vastly disrupted. Further, behavioral criteria for diagnosis are comprised of past failed attempts at abstaining from gambling, depression, physiologically detrimental results, suicidal thoughts surrounding gambling behavior and the contemplation or execution of law breaking as a means by which to pay off gambling debts (Diagnostic and Statistical Manual, 2000).


These behaviors are clearly destructive, as the very criterion by which they are diagnosed outline the devastating outcomes in which they result. It seems to follow naturally, then, that pathological gambling would be explained in a behavioral manner, rather than a neuro-scientific one. This assumption has validity, as gambling is not an intrinsic, ever present problem; rather it relies on situational cues and learned behaviors, in keeping with the somatic marker theory, to instigate episodes of the behavior. Tendency toward acquiring these learned reactions to various cues, and toward developing somatic markers in gambling contexts, however, has been attributed, in part, to these behaviors’ close correlation with the existence of certain genetic and neurological make-up, which appears to have hereditary consequences.


Both behavioral and neuro-scientific research have been examined in tandem in order to draw conclusions about the linkage between the two in their ability to drive gambling and addictive behaviors. Dretsch and Tipples (2008) performed a study in which the Iowa Gambling Test (IGT), one used for research on decision-making processes, was employed to examine the effects of high load on the working memory on the function of somatic markers as targets and cues to particular behaviors. The manipulation of working memory load was accomplished by employing a random number generator so as to increase the difficulty and unpredictability of the various IGT tasks and exhibited a detractive effect on decision-making. (Dretsch & Tipples, 2008). In Clark, et al.’s (2009) research, behavioral results indicated that losses in a slot machine task led to a higher propensity to continue to play; neurological data was collected as well. Event-related potentials in an fMRI were analyzed to find that losses in which the slot reel stopped proximal to what would have been a winning outcome led to very different neural activity patterns than if the reel stopped on an image not near to the image that would have won (Clark, Lawrence, Astley-Jones, Gray, 2009).


The existing literature on pathological gambling suggests that it is centered on a supposed need to continue playing, and an insatiable desire to give it one more chance, until, after an unknowable number of trials, positive feedback is presented in the form of a win, or a negative outcome, such as major loss, presents further opportunity to try harder and with greater frequency. This closely mirrors the process by which action potentials are fired. Voltage thresholds must be reached exactly or in excess in order for channels to open and allow neurotransmitters to convey information from neuron to neuron via their axons, dendrites and axon terminals. It is interesting to note the way in which our physiologic method for conveying information, regulating the body, expressing emotion, activating muscle, and performing vital processes so closely resembles a process that is so completely destructive when it is translated from neuro-scientific to behavioral in nature. The process by which action potentials fire, in which voltage increases until something definitive occurs, differs from gambling and other addictive behavioral disorders in that it is highly stratified and “black and white.” Either there is a response, or there is none, regardless of the amount of voltage put into a system without bringing about a response. Conversly, in addictive behaviors, feedback is constant, until particularly jarring feedback triggers a more action potential-like response.


Works Cited:

Clark, L.; Lawrence, A.J.; Astley-Jones, F.; Gray, N. (2009). Gambling near-misses enhance motivation to gamble and recruit win-related brain circuitry. Neuron, 61(3), 481-490.

Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Washington, DC, American Psychiatric Association, 2000.

Dretsch, M.N.; Tipples, J. (2008). Working memory involved in predicting future outcomes based on past experiences. Brain and Cognition, 66(1), 83-90.

Verdejo-Garcia, A.; Bechara, A. (2009). A somatic marker theory of addiction. Neuropharmacology, 56, 48-62.


Paul Grobstein's picture

brain and gambling

"an insatiable desire to give it one more chance" is a really interesting way to think about compulsive gambling, and yes, it has some metaphoric parallels to the threshhold phenomena of action potential generation.  So, what kind of more complex neural organization could yield that as well as other features of the "behavioral model"?