Understanding Addiction
and treatment options

How Opioids and Alcohol Affect the Brain

Brain regions associated with dependence1

Cortex and limbic systems

Opioid and alcohol dependence are chronic, relapsing brain diseavses that affect both the brain’s cortex and limbic system. Addiction can be devastating both psychologically and physically. While counseling can help patients work through the psychological aspects of dependence, medication may help address the physical changes in the brain.1

The Brain and Pleasure

Endorphin MOA

The limbic system of the brain rewards us for doing life-sustaining activities by releasing endogenous opioids, for example beta endorphins, that attach to opioid receptors in the brain and stimulate the dopamine reward system.2,3 Questions remain about the endogenous opioid system as to the relationship between various opioid peptides and opioid receptors. Endogenous opioids can bind with mu (µ), delta (δ), and kappa (ϰ) opioid receptors.4

The brain and alcohol use

Alcohol MOA

Drinking alcohol can cause an increased release of endogenous endorphins, which can bind to opioid receptors and stimulate the dopamine reward system. For some people, this increased dopamine release can cause them to seek out this feeling again and again.5

The brain and opioid use

Opioid MOA

Heroin and prescription pain relievers are exogenous opioids. When they bind to mu opioid receptors in the brain, the resulting dopamine release can be 2–10 times greater than the dopamine release associated with natural pleasures. This excess of dopamine has a powerful reinforcing effect on the brain, which is why opioids have a high potential for abuse.1

The brain and chronic opioid use

Tolerance development with opioid use over time

Tolerance develops with chronic opioid use. With repeated exposure, opioid receptors become less responsive to opioid stimulation. More opioid is needed to stimulate the reward system to release the same amount of dopamine and produce the same amount of pleasure as before. The cortex sends inhibitory signals to the limbic system to stop an individual from self-destructive behaviors.6 Over time, the limbic system communicates to the cortex that opioid use is important,6 making an individual who is dependent on opioids physically less capable of choosing to avoid risky behaviors.3,7 When an individual who is physically dependent on opioids suddenly stops using, they experience withdrawal symptoms.6

Treating Dependence with Medication

Agonist therapy

Agonist MOA

Agonists bind to mu opioid receptors and fully activate the dopamine reward system so that the patient does not experience withdrawal symptoms. Agonists work similarly to illicit opioids and prescription pain relievers.8

Partial agonist therapy

Partial agonist MOA

Partial agonists bind to mu opioid receptors, blocking them from other opioids and partially activating them. Because they don’t fully activate the opioid receptors, they produce a more limited response than full agonists.9

Antagonist therapy

Antagonist MOA

Opioid antagonists bind to mu opioid receptors in the brain, blocking the receptor from opioids. Antagonists do not activate the mu opioid receptor, so there is no excessive stimulation of the dopamine reward system.6


Binds to µ opioid receptor YES YES YES
Activates µ opioid receptor to release dopamine YES YES
but not to the extent of a full agonist
Administration Daily oral concentration Daily sublingual film, sublingual tablet, buccal film, six-month subdermal implant, or extended-release injection Daily oral medication or monthly intramuscular injection
Setting Provided at certified opioid treatment program settings Sublingual film, sublingual tablet, or buccal film can be initially provided in a physician's office then as a take-home medication. The six-month subdermal implant and extended-release injection require healthcare provider administration Daily oral can be provided as take-home medication. Monthly injection requires HCP administration.
DEA schedule Schedule II controlled substance Schedule III controlled substance Not scheduled
Requires detox NO NO YES
Requires counseling YES YES YES

This chart is not intended to make any product comparisons. No comparisons of safety or efficacy of any products are to be made.

VIVITROL is not right for everyone. There are significant risks from VIVITROL treatment, including risk of opioid overdose, injection site reactions and sudden opioid withdrawal.
See Important Safety Information below. Discuss all benefits and risks with your patients.
See Prescribing Information. Review Medication Guide with your patients.

Request A Representative


Request a visit from a VIVITROL representative to learn more about how VIVITROL may help your opioid- and alcohol-dependent patients.


VIVITROL® Co-pay Savings Program


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  1. National Institute on Drug Abuse (NIDA). Drugs, brains, and behavior: the science of addiction. NIH publication 14-5605. https://d14rmgtrwzf5a.cloudfront.net/sites/default/files/soa_2014.pdf. Revised July 2014. Accessed April 11, 2019.
  2. Esch T, Stefano G. The neurobiology of pleasure, reward processes, addiction and their health implications. Neuro Endocrinol Lett. 2004;25:235-251.
  3. Adinoff B. Neurobiologic processes in drug reward and addiction. Harv Rev Psychiatry. 2004;12(6):305-320.
  4. Meyer JS, Quenzer F. The opioids. In: Psychopharmacology: Drugs, the Brain, and Behavior. 2nd ed. Sunderland, MA: Sinauer Associates, Inc; 2013:305-337.
  5. Herz A. Endogenous opioid systems and alcohol addiction. Psychopharmacology (Berl).1997;129(2):99-111.
  6. Kosten TR, George TP. The neurobiology of opioid dependence: implications for treatment. Sci Pract Perspect. 2002;1(1):13-20.
  7. Goldstein RZ, Volkow ND. Drug addiction and its underlying neurobiological basis: neuroimaging evidence for the involvement of the frontal cortex. Am J Psychiatry. 2002;159(10):1642-1652.
  8. Center for Substance Abuse Treatment (CSAT). Medication-Assisted Treatment for Opioid Addiction in Opioid Treatment Programs. Treatment Improvement Protocol (TIP) Series 43. DHHS Publication No. (SMA) 12-4214. 2005.
  9. Center for Substance Abuse Treatment (CSAT). Clinical Guidelines for the Use of Buprenorphine in the Treatment of Opioid Addiction. Treatment Improvement Protocol (TIP) Series 40. DHHS publication No 04-3939. Rockville, MD: Division of Pharmacological Therapies, Center for Substance Abuse Treatment; 2004.
  10. US Department of Justice, Drug Enforcement Administration. Drug schedules. http://www.dea.gov/druginfo/ds.shtml. Accessed April 11, 2019.
  11. Substance Abuse and Mental Health Services Administration (SAMHSA). Federal Guidelines for Opioid Treatment Programs. HHS Publication No PEP15-FEDGUIDEOTP. http://store.samhsa.gov/shin/content/PEP15-FEDGUIDEOTP/PEP15-FEDGUIDEOTP.pdf. Published January 2015. Accessed April 11, 2019.
  12. Substance Abuse and Mental Health Services Administration. The facts about naltrexone for the treatment of opioid addiction. HHS Publication No. (SMA) 12-4444. Printed 2009; revised 2012.
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