Deep inside your brain, tiny gaps are just waiting for opioids to come along. These opioid receptors work like locks for the key of opioids to fit inside. When an opioid is nestled inside a receptor, chemical reactions that ease pain and boost euphoria begin.
Multiple types of opioid receptors exist, and they all respond when you take a drug like Vicodin or OxyContin.
Your brain needs opioid receptors, as your body makes natural opioids to help ease discomfort. Without those connection points, your pain levels could be intolerable.
But researchers are looking at those receptors change when people take opioid drugs chronically, and how that can contribute to compulsive drug use. With that knowledge, they could design helpful treatment programs that address opioid use disorder (OUD) where it starts.
It's easy to think of the brain as a solid mass of gray matter. In reality, tiny gaps exist between neurons inside your brain. Those little spaces allow for chemical and electrical reactions. Some gaps are studded with opioid receptors.
When opioids enter your brain, they seek out receptors and latch. When the tie forms, chemical reactions begin and chemicals flood the space between neurons.[1]
Researchers have discovered five types of opioid receptors:[2]
Painkiller opioids typically latch to MOR, which are responsible for euphoria. Others are involved. DOR and KOR can ease pain, whereas MOR and DOR offer a mood boost. KOR can also cause feelings of malaise.[3]
Researchers say that opioids are the "drivers of addiction," triggering changes that lead directly to compulsive drug use.[4]
Opioid receptors interact directly with GABA neurons, which modulate the neurotransmitter dopamine.[5] When they're not working, cells are flooded with dopamine, a chemical that can trigger a high.
Humans are genetically programmed to seek out experiences that feel good. If we use drugs and enjoy them, even once, part of our brain will remember that episode and call out for drugs. We may use them again as a result.
But brain cells adapt, with counterreactions that help the brain work even while flooded with dopamine.[6] The first dose we took is no longer strong enough, so we take more. Brain cells adapt again. In time, brain cells become accustomed to a flood of dopamine due to their reactions and adjustments, and without that flood, we can feel physically and mentally unwell.
While chemical reactions are partially responsible for OUD, habits and reinforcement play a role too.
A learned association is also part of the addiction process.[7] You're in pain, you take a pill and the pain goes away. Every time you repeat this process, the connection between taking a pill and pain relief grows stronger.
If you misuse opioids without pain, the euphoria becomes the reinforcing trigger.[8] You take the drug, and it makes you feel great. Every time you feel great, your brain learns that drugs are responsible for that feeling.[9]
The most effective treatment programs blend therapies to ease chemical imbalances and help you reverse learned associations. Medication for Addiction Treatment (MAT) programs work like this, combining the use of medications and therapy into a comprehensive program.
Medications like Suboxone (buprenorphine/naloxone) latch imperfectly to opioid receptors in the brain; they do enough to ease chemical imbalances so you're not overwhelmed with cravings, but not enough to trigger the massive flood of dopamine that stronger opioid drugs do.[10] Therapy helps you find other approaches (exercise, conversation or food) to improve your mood and help you deal with relapse triggers.
If you're struggling to quit opioids, ask your doctor if MAT is right for you.
Peter Manza, PhD received his BA in Psychology and Biology from the University of Rochester and his PhD in Integrative Neuroscience at Stony Brook University. He is currently working as a research scientist in Washington, DC. His research focuses on the role of the brain dopamine system in substance use disorders and in aging. He also studies brain function in obesity and eating disorders.
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