ADC 655 Module 2 How Drugs Act on the Brain Example

Reviewed by Frances Ledbetter, MA Aspen University Updated October 2026

This ADC 655 Module 2 sample paper explains how drugs with very different chemistry produce addiction through common brain mechanisms, for a composite psychoeducation group in Colorado whose members use alcohol, opioids, methamphetamine and cannabis. Aspen University's course on the neurobiology of addiction asks students in this module to understand drug actions. Di Chiara and Imperato found that drugs abused by people raised dopamine in the brain's mesolimbic reward pathway in rats. Lüscher and Ungless classified addictive drugs by how they produce that rise: by acting on receptors, by disinhibiting dopamine neurons or by blocking dopamine's removal. Nestler described molecular changes shared across drugs that may help explain why addiction lasts.

CourseADC 655 Neurobiology of Addiction
ModuleModule 2
Paper typeMechanisms paper
LengthAbout 1,044 words, 6 pages
FormatAPA 7 student paper
SchoolAspen University
ProgramPsychology and Addiction Studies
UpdatedOctober 2026

Free sample paper for ADC 655 Module 2

1

Different Doors, Same Room: How Drugs With Different Targets Converge on the Reward System

Student Name

Psychology and Addiction Studies Program, Aspen University

ADC 655: Neurobiology of Addiction

Instructor Name

Month Day, Year

What this page is doingThe title's image captures how varied drugs reach a common circuit. APA 7 student title page.
2

Different Doors, Same Room: How Drugs With Different Targets Converge on the Reward System

At her next psychoeducation group at the Colorado Springs residential program, Nadia, the counselor introduced in the previous paper, faced a question from Teresa, who was in treatment for alcohol: "Marcus uses meth, Jay uses pills, I drink. Is it really the same thing?" The counselor, her program and her group are all fictional; the sections below review how drugs act on the brain to answer her.

A Common Effect

Di Chiara and Imperato (1988) used a technique called microdialysis to measure dopamine in the brains of freely moving rats given various drugs. Drugs that people commonly misuse, including opioids, ethanol, nicotine, amphetamine and cocaine, increased dopamine concentrations in the mesolimbic system, especially in the nucleus accumbens, more than in other dopamine regions. Drugs that people do not typically misuse did not have this effect. The study provided strong evidence that addictive drugs, despite very different chemical structures and primary targets, share an effect on a common reward circuit.

Different Routes to the Same Effect

Lüscher and Ungless (2006) proposed classifying addictive drugs by the mechanism through which they increase dopamine. One group, including nicotine, acts on receptors located directly on dopamine neurons in the ventral tegmental area, increasing their activity. A second group, including opioids, cannabinoids and gamma-hydroxybutyrate, acts on receptors of inhibitory neurons that normally restrain dopamine neurons, so that dopamine neurons are disinhibited. Alcohol and benzodiazepines act through similar disinhibition among their effects. A third group, including cocaine, amphetamines and ecstasy, acts on the dopamine transporter, the protein that removes dopamine from the synapse, either blocking it or reversing it, so that dopamine accumulates. The classification explains how such varied drugs reach the same outcome.

DrugMain targetHow dopamine risesOther important effects
AlcoholSeveral, including GABA receptorsPartly by disinhibiting dopamine neuronsSedation; dangerous withdrawal
Opioids, such as heroin and oxycodoneOpioid receptorsDisinhibiting dopamine neuronsSlowed breathing; overdose
MethamphetamineDopamine transporterReversing the transporter, releasing dopamineOverheating, heart strain, psychosis
CocaineDopamine transporterBlocking reuptakeHeart strain; seizures
CannabisCannabinoid receptorsDisinhibiting dopamine neuronsMemory and coordination effects
What this page is doingEach drug opens a different door, but every door leads into the same room.
3

Changes With Repeated Use

A single dose raises dopamine briefly. Addiction involves changes that last long after the drug is gone. Nestler (2005) reviewed evidence for molecular changes shared across drugs of abuse in reward-related brain regions. One example is deltaFosB, a transcription factor, a protein that regulates which genes are active, which accumulates gradually in neurons of the nucleus accumbens with repeated exposure to many drugs and persists for weeks. In animal studies, increasing deltaFosB made animals more sensitive to drugs' rewarding effects. Other shared changes involve signaling pathways that alter how neurons respond to dopamine and glutamate. Nestler argued that these common molecular adaptations may help explain the shared features of addiction across drugs, including persistent craving and relapse.

Differences Matter Too

The shared mechanism does not make all drugs alike. Their other actions produce different effects and dangers: opioids can stop breathing, alcohol withdrawal can cause seizures, methamphetamine can cause psychosis and overheating. Treatment differs as well, since medications exist for opioid and alcohol use disorders but not for stimulant use disorders. Shared neuroscience is a reason for common understanding, not identical treatment.

Beyond Dopamine

Dopamine is only part of the story. Drugs also act on glutamate, the main excitatory messenger, and on the brain's stress systems, and these actions contribute to craving and relapse, as later modules will show. Opioids act on the brain's own opioid system, which is involved in pain and pleasure. Alcohol acts on several systems at once. A full account of any drug's effects requires looking beyond the dopamine story that unites them.

Tolerance and Sensitization

Repeated use produces two opposite kinds of change. Tolerance means that the same dose produces less effect, which is why people often use more over time. Sensitization means that some responses grow stronger with repetition; Berridge and Robinson's work suggests that the wanting response to drug cues can sensitize even as the pleasurable effect undergoes tolerance. The combination of growing wanting and shrinking pleasure fits what many clients describe.

The Role of the Nucleus Accumbens

The nucleus accumbens, the region where Di Chiara and Imperato measured the largest dopamine increases, sits at a crossroads between brain areas involved in emotion, memory and action. It helps translate motivation into behavior. Its central role in drug effects helps explain why drugs so powerfully shape what people want and do, and why cues linked to drug use can trigger strong urges long after use stops.

Explaining It to the Group

Nadia answered Teresa with an image: the brain's reward system is a room, and each drug finds its own door into it. Alcohol and pills unlock the door by quieting the guards; meth and cocaine prop the door open so the dopamine cannot leave. Once in the room, all of them leave marks that make the brain want to go back. She added that the differences matter for safety: Teresa's alcohol withdrawal and Jay's opioid overdose risk needed specific medical attention. But the shared room meant they could share recovery tools, such as managing cues and building other rewards, and learn from one another in the group.

Questions Nadia Expects Next

Nadia expected follow-up questions after the session, so she prepared answers in advance. If Jay asked why pills felt calmer than meth, she would point to the receptor differences in the drug-class table: opioids act through their own receptors before dopamine rises, while stimulants act on the dopamine transporter itself (Lüscher & Ungless, 2006). If Teresa asked whether drinking could really change her brain the way meth had changed Marcus's, she would describe the gene-level changes Nestler (2005) found across drug classes, which build slowly with heavy use and also fade slowly once it stops.

Conclusion

Di Chiara and Imperato showed that addictive drugs share an effect on dopamine in the mesolimbic system, Lüscher and Ungless classified the routes by which they produce it and Nestler described molecular changes common across drugs that may underlie lasting addiction. For Nadia's group, the science explained why their different drugs produced similar struggles and why they could work on recovery together while respecting each drug's particular dangers.

References

Di Chiara, G., & Imperato, A. (1988). Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats. Proceedings of the National Academy of Sciences, 85(14), 5274-5278. https://doi.org/10.1073/pnas.85.14.5274

Lüscher, C., & Ungless, M. A. (2006). The mechanistic classification of addictive drugs. PLoS Medicine, 3(11), Article e437. https://doi.org/10.1371/journal.pmed.0030437

Nestler, E. J. (2005). Is there a common molecular pathway for addiction? Nature Neuroscience, 8(11), 1445-1449. https://doi.org/10.1038/nn1578

ADC 655 Module 2 instructions, in plain terms

The second module of ADC 655 typically asks for a paper on how drugs act on the brain. Work from the Module 2 instructions in your Aspen course; the group here is fictional. Explain the evidence that addictive drugs share effects on reward circuitry, describing at least one key experiment. Describe how different classes produce those effects, grouping them by mechanism. Explain molecular changes with repeated use and why they might make addiction last. Note differences between drugs as well as similarities, especially in withdrawal and overdose risk. Translate the science for a client audience if your prompt calls for it, using images that keep the key points intact. Use APA 7 for every source, and define technical terms on first use. A table of drug classes and targets helps readers compare mechanisms at a glance.

How this ADC 655 Module 2 example is built

Nadia, the composite counselor, leads a group whose members use different substances and ask whether their addictions are "the same thing." A 1988 experiment by Di Chiara and Imperato shows drugs abused by humans raising dopamine in the nucleus accumbens of rats. Lüscher and Ungless's PLoS Medicine article classifies drugs into receptor-acting, disinhibiting and transporter-acting groups. Nestler's Nature Neuroscience article describes shared molecular changes such as the accumulation of deltaFosB. A five-row table lists drug classes, targets and how each raises dopamine. The group explanation uses doors into one room, and differences in withdrawal and overdose risk are flagged for safety.

Reading the ADC 655 Module 2 grading rubric

Mechanisms papers earn credit for accurate descriptions of drug actions, a clear account of shared and distinct effects and translation that respects complexity. This example uses a foundational experiment and a modern classification to show convergence on dopamine. Molecular changes are explained with a review, connecting a drug's effect in the moment to changes that last for weeks. Differences between drugs, such as withdrawal dangers, are noted so the shared mechanism is not overstated. The group explanation is simple and accurate, and it ends with a practical point: shared mechanisms mean shared recovery tools.

ADC 655 Module 2 help from the desk

Mechanisms papers often stop at "drugs release dopamine," which hides the differences that matter for safety and treatment. Explain how each class does it, since the routes differ and the differences matter. Note that drugs also act on other systems, which explains different effects and dangers. Connect acute action to changes with repeated use, such as tolerance and sensitization. Avoid implying all addictions are identical; withdrawal, overdose risk and treatment differ by drug. When translating for clients, use images that preserve the key points. Remind clients that shared brain mechanisms also mean shared recovery tools. Check with medical staff before describing withdrawal risks, since details vary by drug and person.

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 2 questions, answered

What does ADC 655 Module 2 usually ask for?

Aspen's ADC 655 covers how drugs act on the brain in this module, so a paper on drug mechanisms and their convergence on reward circuitry is typical. Check your Module 2 prompt.

Do all addictive drugs increase dopamine?

Di Chiara and Imperato found that drugs abused by humans increased dopamine in the mesolimbic system of rats, though they do so by different mechanisms.

How are addictive drugs classified by mechanism?

Lüscher and Ungless grouped them into drugs acting on receptors, drugs that disinhibit dopamine neurons and drugs acting on dopamine transporters.

Where can I find a free ADC 655 Module 2 sample paper?

This page holds the full paper: shared effects on dopamine, a classification of drugs by mechanism and molecular changes with repeated use.

What is deltaFosB?

A protein that accumulates in reward-related brain cells with repeated drug use and may contribute to long-lasting changes, as Nestler describes.