| Course | ADC 655 Neurobiology of Addiction |
|---|---|
| Module | Module 3 |
| Paper type | Neurobiology model paper |
| Length | About 1,022 words, 6 pages |
| Format | APA 7 student paper |
| School | Aspen University |
| Program | Psychology and Addiction Studies |
| Updated | October 2026 |
Free sample paper for ADC 655 Module 3
From Getting High to Feeling Normal: The Three-Stage Cycle of Addiction in the Brain
Student Name
Psychology and Addiction Studies Program, Aspen University
ADC 655: Neurobiology of Addiction
Instructor Name
Month Day, Year
From Getting High to Feeling Normal: The Three-Stage Cycle of Addiction in the Brain
During one of Nadia's Thursday groups at the residential program from earlier papers, a client named Jay said something that caught Nadia's attention. He had started oxycodone after a knee injury, liked it at first and now, years later, felt nothing like the early highs. "I don't use to get high anymore," he said. "I use so I don't feel like garbage." Jay, Nadia and the program are fictional. His words describe, almost exactly, the cycle that neuroscience research has mapped.
A Cycle in Three Stages
Koob and Volkow (2010) reviewed the neurocircuitry of addiction and proposed that addiction is a cycle of three stages that worsens over time. During bingeing and intoxication, the substance engages reward circuits in the basal ganglia, including the nucleus accumbens, releasing dopamine and opioid peptides; cues linked to the drug acquire motivational power. In the withdrawal and negative affect stage, reward function declines and the brain's stress systems in the extended amygdala, including corticotropin-releasing factor and dynorphin, become more active, producing irritability, anxiety and dysphoria when the drug is absent. In the preoccupation and anticipation stage, often called craving, the prefrontal cortex, which supports planning and self-control, functions poorly, while glutamate signals from cortex to reward regions drive drug seeking in response to cues and stress. Each pass through the cycle strengthens the changes, so that the cycle intensifies.
| Stage | Main brain systems | Jay's experience | Treatment target |
|---|---|---|---|
| Binge and intoxication | Basal ganglia; dopamine and opioid peptides | Early highs, now faint | Medications that block or replace the drug's action |
| Withdrawal and negative affect | Extended amygdala; stress systems | "I feel like garbage" without it | Managing withdrawal; treating stress and mood |
| Preoccupation and anticipation | Prefrontal cortex; glutamate projections | Thinking about the next dose, planning around supply | Building control; cue and stress management |
| Across stages | Habit circuits | Using on autopilot at set times | New routines; breaking habit chains |
From Pleasure to Relief
A central idea in Koob and Volkow's model is a shift in why people use. Early in addiction, drug use is driven largely by positive reinforcement: it produces pleasure. Over time, as reward systems are blunted and stress systems heightened, use is increasingly driven by negative reinforcement: it relieves the distress of withdrawal and the low mood that persists between doses. Jay's statement that he uses so he does not feel like garbage describes negative reinforcement precisely.
From Actions to Habits to Compulsion
Everitt and Robbins (2005) described a related shift in how drug seeking is controlled. Early on, seeking a drug is a goal-directed action: a person does it because they expect a desired outcome. With repetition, control shifts from the ventral striatum, involved in goal-directed motivation, toward the dorsal striatum, involved in habits, so that seeking becomes a habit triggered by cues regardless of whether the outcome is still wanted. They argued that compulsive drug use, continued despite serious harm, may arise when these habits combine with weakened prefrontal control. Jay's description of taking pills at the same times each day, "without thinking," reflects this habitual stage.
What the Cycle Means for Treatment
Volkow et al. (2016) summarized the implications of this model. Because addiction involves reduced sensitivity to natural rewards, heightened stress reactivity and weakened executive control, treatment must address more than the drug's rewarding effects. They argued that medications, behavioral therapies and supports should be chosen to target specific stages: medications such as buprenorphine stabilize the opioid system and reduce withdrawal; stress management and treatment of mood problems address negative affect; and behavioral therapies strengthen control and help manage cues. They also emphasized that the brain changes are not permanent and that recovery is possible, though it takes time.
Why the Stages Reinforce Each Other
The stages do not simply follow each other; they feed one another. Each binge strengthens cue-reward associations and deepens the stress-system changes that make withdrawal worse. Worse withdrawal adds negative reinforcement to the reasons for using. Weakened prefrontal control makes it harder to resist the cues and distress that drive the next binge. This mutual reinforcement explains why addiction often worsens over time and why breaking the cycle at any one point, such as stabilizing withdrawal, can make change at the others easier.
Explaining the Cycle to Jay
Nadia drew the cycle as a circle on the whiteboard and asked Jay where he was. He pointed to the second stage. She explained that his experience was not a sign of weakness but of a brain whose stress system had become overactive and whose reward system had dulled, so that oxycodone now mainly relieved distress the drug itself had helped create. She explained that his prescriber's plan to start buprenorphine would calm the withdrawal stage, that groups on stress and cravings would address the other stages and that the circuits could rebalance over months.
The Role of Stress Systems
The second stage deserves particular attention because it explains much of the suffering in established addiction. Koob and Volkow describe the recruitment of stress chemicals such as corticotropin-releasing factor and dynorphin, which produce anxiety, irritability and low mood during withdrawal and can persist long after acute withdrawal ends. This protracted distress helps explain why people relapse weeks or months after stopping, and why treating mood, anxiety and stress is central to recovery rather than an optional extra.
Limits of the Model
The model is drawn largely from animal research and brain imaging, and it describes a general pattern rather than every person's experience. Some people who use drugs heavily do not move through all stages; others recover without treatment. The model is a map, not a destiny, and its value for clients lies in making their experience understandable.
Conclusion
Koob and Volkow describe addiction as a repeating circle of using, feeling worse without the drug and then craving it, in which motivation shifts from pleasure to relief. Everitt and Robbins add a shift from goal-directed actions to habits. Volkow, Koob and McLellan show how each stage points to treatment. For Jay, the model explained why he now uses to feel normal and what can break the cycle.
References
Everitt, B. J., & Robbins, T. W. (2005). Neural systems of reinforcement for drug addiction: From actions to habits to compulsion. Nature Neuroscience, 8(11), 1481-1489. https://doi.org/10.1038/nn1579
Koob, G. F., & Volkow, N. D. (2010). Neurocircuitry of addiction. Neuropsychopharmacology, 35(1), 217-238. https://doi.org/10.1038/npp.2009.110
Volkow, N. D., Koob, G. F., & McLellan, A. T. (2016). Neurobiologic advances from the brain disease model of addiction. New England Journal of Medicine, 374(4), 363-371. https://doi.org/10.1056/NEJMra1511480
ADC 655 Module 3 instructions, in plain terms
The third module of ADC 655 typically asks for a paper on the stages of the addiction cycle. Follow the Module 3 instructions in your Aspen course; the client here is fictional. Describe each stage and the brain systems involved, naming specific regions and chemical messengers. Explain the shift from positive to negative reinforcement and from goal-directed to habitual behavior. Use a primary source for the model rather than a textbook summary. Show how each stage appears in one person's story, then say what treatment offers at that stage, including medications and behavioral approaches. Give APA 7 references for every source, and keep the neuroscience accurate while explaining it in plain terms where a client is involved. Note the limits of the model, since it describes a general pattern and not every person's path.
Inside the ADC 655 Module 3 example
Jay, a composite client at the Colorado Springs program, tells Nadia, his counselor, that he uses oxycodone "just to feel normal." Koob and Volkow's Neuropsychopharmacology review describes the three stages and their brain systems. Everitt and Robbins's Nature Neuroscience article explains the move from actions to habits to compulsion, linked to a shift from ventral to dorsal striatum. The 2016 review by Volkow, Koob and McLellan connects the stages to treatment. A four-row table links each stage to its circuits, Jay's experience and a treatment target. The explanation shows Jay that feeling normal through opioids is the second stage of the cycle at work, and that each stage has a treatment target.
Where the marks sit in the ADC 655 Module 3 rubric
Addiction cycle papers earn credit for an accurate model, clear links between stages and brain systems and practical implications. This example describes each stage with its circuits and neurochemistry, citing the review that proposed the model. The shift to negative reinforcement is explained as the core of chronic addiction. Everitt and Robbins's habit account adds a complementary view of how drug seeking becomes automatic. The table makes the model usable. The application turns Jay's phrase into a teaching point, and the treatment implications address each stage rather than only the high. The limits section keeps the model from sounding like destiny.
ADC 655 Module 3 help: mistakes that cost marks
Addiction cycle papers often describe only the high. Give equal weight to withdrawal, negative affect and preoccupation, which dominate later addiction. Name the brain systems accurately. Explain negative reinforcement clearly: using to escape a bad state, which is different from using for pleasure. Connect stages to treatment, so the model leads somewhere practical. Use the client's own words to illustrate the model. Avoid suggesting the cycle cannot be broken; each stage has treatment targets, and naming them gives clients somewhere to start. Draw the cycle for clients and ask where they are; most recognize their stage at once.
Write yours, or have the desk draft it
This paper is an original model document written by our desk, not a submitted student paper and not an official Aspen University document. Read it for the moves, then write your own to the instructions in your classroom. If you want one built to your exact prompt and rubric, the first custom sample is free and arrives in 24 to 48 hours.
More ADC 655 and Psychology and Addiction Studies sample papers
- ADC 655 Module 1: The Brain's Reward System
- ADC 655 Module 2: How Drugs Act on the Brain
- ADC 655 Module 4: Animal Models of Addiction
- ADC 655 Module 5: Neuroimaging in Addiction
- ADC 655 Module 6: Stress, Withdrawal and Craving
- ADC 655 Module 7: Relapse Research
- ADC 655 Module 8: Genetics and Implications for Treatment
- PAC 240 Module 1: The Helping Relationship in Addiction Work
- PSY 540 Module 4: Individual Supervision
- ADC 510 Module 2: Theories of Addiction
- PAC 411 Module 7: Populations at Risk
ADC 655 Module 3 questions, answered
What does ADC 655 Module 3 usually ask for?
Aspen's ADC 655 covers the stages of the addiction cycle in this module, so a paper on the three stages, their brain systems and treatment implications is typical. Look at your Module 3 prompt.
What are the three stages of the addiction cycle?
Koob and Volkow name a binge stage, a stage of withdrawal with low mood and a stage of preoccupation with the next use, each involving different brain systems.
Why do people use drugs to feel normal?
In the withdrawal and negative affect stage, stress systems are overactive and reward systems blunted, so using relieves distress rather than producing pleasure, a form of negative reinforcement.
Where can I find a free ADC 655 Module 3 sample paper?
This page has the full paper: the three stages of the addiction cycle, the shift to habits and a table linking stages to treatment.
What is the shift from actions to habits in addiction?
Everitt and Robbins describe drug seeking moving from deliberate, goal-directed behavior to habit and then compulsion, as control shifts between parts of the striatum.