Opioids are the body’s natural painkillers. They also cause sedation and depress respiration. Endogenous (ie. naturally occurring) opioids include endorphins, enkephalins, dynorphins, and endomorphins, each a sub-class of compounds that interact with the opioid system. In addition to pain-killing, opioids are involved in reward, and thus addictive behaviors.
Opiates, on the other hand, are compounds derived from the poppy plant including opium, morphine, heroin, and synthetic drugs like hydrocodone. These stimulate the opioid system and induce a high because they have molecular structures that are so similar to the body’s natural opioids that they “impersonate” opioids, dock with opioid receptors and stimulate both the opioid and dopamine systems.
Dopamine and and opioid receptors belong to the same family of neural receptors, which neuroscientists call the “G protein-coupled receptor superfamily,” which may be one of the reasons they are both involved in reward and addiction.1 Research has found that alcohol intake releases beta-endorphins, a kind of natural morphine2 and alcohol abusers have low chronic levels of beta-endorphins.3
In a study involving rodents, researchers found that low and moderate alcohol intake released endorphins in the Ventral Tegmentum Area (VTA), a key part of the Reward System. Interestingly, high doses of alcohol didn’t.4
There are three opioid receptors, dubbed the mu, delta and kappa receptors. Of these three receptors, the mu receptor is suspected to play opioids’ biggest role in addiction. Genetically-altered mice bred to have no mu-opioid receptors did not obtain the pain-killing properties normally found when given morphine, nor did they get addicted to morphine, unlike mice with mu receptors. These mu-deficient mice also found alcohol, marijuana and nicotine less rewarding.5
Blocking opioid receptors was also found to consistently reduce alcohol use in experiments involving non-human primates.6
Monkeys who had a particular mutation to their mu receptors (the “118 G-mu-opioid receptor variant”) demonstrated increased euphoria from alcohol compared to monkeys without the variant,7 and also had greater cravings after alcohol exposure,8 both indications of increased risk of drug dependence. Scientists are investigating whether this mutation in humans may be a bio-marker for increased risk of addiction.
For the next article in the Non-Dopamine Neurotransmitters series click here.
1. Molecular and Cellular Basis of Addiction, Science Magazine, October 3, 1997.
2. The G Allele of the Mu-Opioid Receptor Gene Is Linked to Craving for Alcohol, medicalnewstoday, January 7, 2007.
3. Alcohol Abuse Is Hereditary, medicalnewstoday, July 5, 2007.
4. “Feel-Good’ Endorphins in the Brain Released By Low to Moderate But Not Heavy Drinking, medicalnewstoday.com, March 21, 2009.
5. Determining How the Opioid System Controls Pain, Reward and Addictive Behavior,medicalnewstoday.com, October 15, 2007.
6. A Range of Research-Based Pharmacotherapies for Addiction, Science Magazine, October 3, 1997.
7. Study Advances Evidence For Receptor’s Role in Alcohol Pleasure and Problems, medicalnewstoday, March 10, 2007.
8. The G Allele of the Mu-Opioid Receptor Gene Is Linked to Craving for Alcohol, medicalnewstoday, January 7, 2007.