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Neuroscience of Internet Pornography Addiction: A Review and Update. Neurobiology of Addiction. All drugs of abuse affect the mesolimbic dopamine (DA) pathway, which originates from the ventral tegmental area (VTA) and projects into the nucleus accumbens (NAcc).

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Commonly called the reward center, the NAcc is heavily connected with pleasure, reinforcement learning, reward seeking, and impulsivity. The mesolimbic dopamine pathway connects with three other key regions to form a collection of integrated circuits commonly called the reward system: The amygdala (positive and negative emotions, emotional memory), hippocampus (processing and retrieval of long term memories), and the frontal cortex (coordinates and determines behavior). Taken together, the reward system and its connecting regions modulate, among other things, pleasure, reward, memory, attention, and motivation .

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The past decade has yielded multiple theories of addiction, all of which involve the reward system and related brain regions and substrates . Three- Stage Model of Addiction Nora Volkow describes addiction as a neurobiochemically based shift from impulsive action learned through positive reinforcement to compulsive actions learned through negative reinforcement .

This in turn is seen as leading to an addictive cycle that progressively worsens over time. Volkow, Wang, Fowler, Tomasi and Telang . Different classes of drugs activate the reward system through different means, however, the universal result is a flood of dopamine in the NAcc (reward center).

This results in acute positive reinforcement of the behavior that initiated the flood. In this impulsive stage, this positive reinforcement results in addictive related learning associations . Neuroplastic changes begin to occur, however, as the continued release of dopamine in the NAcc leads to an increase in dynorphin levels.

Dynorphin, in turn, decreases the dopaminergic function of the reward system, resulting in a decrease of the reward threshold and an increase in tolerance . The resulting negative emotional state leads to activation of brain stress systems and dysregulation of anti- stress systems. This leads to a decreased sensitivity to rewards and an increase in the reward threshold, which is called tolerance. This further progresses to negative reinforcement as the individual continues to engage in the addictive behaviors to avoid the negative affect associated with withdrawal.

This, in turn, encourages the reinstatement and/or reinforcement of the addictive behaviors. Here, the impulsive behavior shifts to compulsive behavior, referred to in the model as chronic taking/seeking . A key point of this stage is that withdrawal is not about the physiological effects from a specific substance. Rather, this model measures withdrawal via a negative affect resulting from the above process. Aversive emotions such as anxiety, depression, dysphoria, and irritability are indicators of withdrawal in this model of addiction . Researchers opposed to the idea of behaviors being addictive often overlook or misunderstand this critical distinction, confusing withdrawal with detoxification . Like the mesolimbic DA pathway, the mesocortical DA starts in the VTA, however it terminates in the frontal cortex.

Specific affected areas within the prefrontal cortex include the dorsolateral prefrontal cortex (DLPFC), responsible for key components of cognition and executive function, and the ventromedial prefrontal cortex (VMPFC) responsible for components of inhibition and emotional response. Taken together, the mesocortical dopamine pathway affects the cognitive component of reward processing .

The neuroplastic impairments expand beyond the mesocortical dopamine pathway into other regions of the prefrontal cortex responsible for motivation, self- regulation/self- control, delayed reward discounting, and other cognitive and executive functions . Goldstein and Volkow . The I- RISA model integrates the increased salience of learned drug- related cues (resulting from the aforementioned positive and negative reinforcement of the addictive behavior) with newly developed deficiencies in top- down inhibitory control. This leaves the individual vulnerable to reinstatement of the behavior, and two primary mechanisms have been identified; cue- induced reinstatement and stress- induced reinstatement . Numerous neuroimaging studies substantiate this model . Anti- Reward George Koob proposed an expansion of the second stage of addiction.

In the opponent- process model of motivation, a- processes reflect positive hedonic effects and b- processes reflect negative hedonic effects. The application in addiction is that a- processes occur first and reflect tolerance. In contrast, the b- processes arise after the a- process have concluded and reflect withdrawal. Solomon and Corbit .

As they repeat the behavior, the balance shifts such that experienced skydivers experience some fear when they jump but great relief when they land. This model has recently been proposed to explain the occurrence of non- suicidal self- injury (“cutting”) . Steps one and two of the three stage model involve “within- system changes”, marked by decreased reward system function, consisting of an increased reward threshold and a decreased natural release of dopamine to non- addictive rewards. Koob expands the model to incorporate “between- system changes”, based largely on the concept of opponent- processes. Specifically, the “Anti- Reward” theory posits that when the brain reward system is engaged, there is a parallel engagement of the brain stress systems for the purpose of limiting the reward response and the maintenance of homeostatic balance with the reward system, resulting in the activation of both the body’s stress system (the hypothalamic- pituitary- adrenal axis), and the brain’s stress system (corticotrophin- releasing factor (CRF)) system.

The aforementioned elevated levels of dynorphin further elevate CRF, and the engagement of these systems brings about many of the negative affects linked to the withdrawal stage. Compounding the problem, the brains anti- stress system also becomes dysregulated, as evidenced by decreases in neuropeptide Y (a natural anxiolytic in the brain). The addicted brain enters an “allostatic” state when the reward system is unable to return to its homeostatic (normal) state. The reward system subsequently develops an altered set- point, leaving the individual vulnerable to relapse and dependence. This is what Koob calls the “dark side” of addiction .

Neurobiology of Learning, Habit, and Motivation While both the Anti- Reward and I- RISA models include learning components, other theories of addiction focus primarily on the learning aspects of addiction, and the biological underpinnings thereof. Everitt and Robbins . Their model includes a combination of classical Pavlovian stimulus- response conditioning and instrumental learning, and they presented evidence illustrating a shift in brain activity from the ventral striatum (location of the NAcc) to the dorsal striatum (brain region established for compulsive behaviors) through the course of the development of addiction. Robinson and Berridge .

The Incentive Salience theory follows the framework of a hypersensitized mesocorticolimbic DA pathway, however, this theory focuses on the motivational attributions attached to the behavior, rather than pleasure or reward . This model perhaps best follows the evolutionary function of the reward system, wherein “drugs induce a false signal of a fitness benefit, which bypasses higher- order information processing” .

This theory explicitly differentiates “liking” and “wanting” in that the development of addiction progresses along a path of liking (hedonic reward value) to wanting (motivational adjustment based on salience) . The researchers thus refer to addiction as a “pathological motivation” .