Synaptic Plasticity and Opioids

Opioids Neurobiological Effects on Synaptic Plasticity

Synaptic plasticity is your brain’s way of communicating with neurons and other neurological systems. Opioids disrupt that system. Get more info now.

SYNAPTIC PLASTICITY AND OPIOIDS

Synaptic Plasticity and Opioids

Opioids Neurobiological Effects on Synaptic Plasticity

Synaptic plasticity is your brain’s way of communicating with neurons and other neurological systems. Opioids disrupt that system. Get more info now.

The information presented on this page is a general overview and is offered here as a comprehensive resource. At Ampelis Recovery, our programs are customized and tailored to the individual’s needs. Specific details below that cover treatment protocols may not reflect the protocols used for our clients.

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What is Synaptic Plasticity?

Synaptic plasticity refers to the brain’s ability to change and adapt at a synaptic level. Synapses are the connections between neurons and allow neurons to communicate. Imagine neurons as neighbors writing letters to each other. Synapses are the mail courier running back and forth between the houses to deliver vital information. Communication between neurons occurs in a fraction of a second. A high level of synaptic plasticity is required for the brain to function clearly.1

Drug-Induced Synaptic Plasticity

Drug-induced synaptic plasticity is the connection between drugs and synaptic plasticity. Specifically, it focuses on the method that drugs use to change the brain. Science suggests a link between drugs and the mesocorticolimbic dopamine system.

The mesocorticolimbic system controls, among other things, motivation and goal-orientated action. Drug-induced synaptic plasticity changes how neurons in this region of the brain communicate with each other. Over time, drug-induced synaptic plasticity can positively or negatively affect the brain depending on the drug, frequency of use, and potency.2

Learn More About Healing the Brain


  • Holistic Approach
  • Brain Chemistry
  • Positive Psychology

What are Opioids?

Opioids include natural and synthetic compounds that bind to opioid receptors and affect GABA receptors in the brain. The shared effects among opioids are euphoria, relaxation, and drowsiness. Drugs in the opioid family include morphine, heroin, and oxycodone.3

What Are They Used For?

Opioids are prescribed for pain relief or administered as a surgical anesthetic. They are typically prescribed for the short term to help with pain related to surgery, trauma, and illness.

In terms of illicit use, people can use opioid drugs to get high. The side effect of euphoria contributes to the high rate of opioid substance abuse.

How Do They Work?

Opioids bind to opioid receptors in the brain. Once stimulated, opioid receptors produce calming, euphoria effects and full-body pain relief. The intense feelings produced by opioids speak both to the drug’s efficacy and addictive risk. Opioids also impact GABA receptors, a multipronged neurological chemical. GABA works to counteract the effects of anxiety, fear, and overstimulation. When activated, GABA creates a subdued feeling.

How Do Opioids Effect Synaptic Plasticity?

Opioids, like other drugs, directly impact synaptic plasticity – albeit on a higher level than average. Opioids change the mesocorticolimbic DA, resulting in the brain adjusting its long-term focus to favor the opioid.

Opioids accomplish this by disrupting the synapses and, consequently, the communication between neurons. A change this drastic takes prolonged opioid abuse to develop fully. However, the synaptic disruption caused by even short-term opioid use lays the groundwork for further changes. Drug-induced synaptic plasticity leads to substance dependency and reduced cognitive performance. Substance dependency is a compounding disease that rewires synaptic plasticity over time.

The negative changes that opioids cause due to synaptic rewiring can reverse, but this process takes treatment and time.

What is Neuroplasticity?

Neuroplasticity refers to the changing nature of neurons. It occurs when new information or experience is gained. It also happens when someone is faced with a problem or unfamiliar setting. Essentially any change can trigger a shift in neuroplasticity. Much like synaptic plasticity, a certain level of neuroplasticity is required for proper brain function and clear thought.

Neuroadaptations

Neuroadaptation occurs when the brain adjusts to maintain healthy function. When a drug enters the brain, it changes the chemical balance. For example, mood-altering drugs such as alcohol increase dopamine chemicals in the brain. Over time, the brain makes less dopamine in expectance that more alcohol will be consumed. The adjustment that occurs from substance use is considered a neuroadaptation.4

Positives Associated with Pleasure

Positive neuroadaptation occurs when the brain changes in response to drug-induced pleasure. It is theorized that when a reward is obtained naturally, i.e., from accomplishment, enjoyment, etc., the brain counteracts these positive chemicals with tempered amounts of GABA to balance out dopamine function and mood. However, drug use disrupts the natural counterbalance causing an overabundance of dopamine and reward. These changes lead to the brain prioritizing drug use over almost anything else.5

Negatives Associated with Withdrawal

Negative neuroadaptations occur most often during withdrawal. In the state of withdrawal, the brain depletes certain mood-stabilizing hormones such as dopamine. Prolonged drug use reduces natural dopamine production. There is little to counterbalance the negative feelings or moods associated with withdrawal because of the reduced dopamine. As such, the user depends on the drug to produce mood-stabalizing hormones and feel “normal.”

Lack of dopamine and other mood stabilizers increases the risk of depression, insomnia, and suicidal ideation, making the body more prone to infection.6

Opioids Neurobiological Effects on Synaptic Plasticity in the Ventral Tegmental Area

What is the Ventral Tegmental Area?

The ventral tegmental area (VTA) is a brain system centered around reward and motivation. The ventral tegmental area communicates directly with the mesocorticolimbic system to produce dopamine. Studies have also drawn a conclusive link between the ventral tegmental area and the development of addiction.

How Do Opioids Affect the VTA?

Opioids rewire the ventral tegmental area by causing an overproduction of dopamine and other feel-good chemicals in the brain. The overproduction causes synaptic plasticity damage, which in turn disrupts neuron communication. Opioids effects on the VTA cause severe behavioral changes such as cravings, changes to interest and hobbies, and de-prioritization of relationships.

In the long-term, the changes on the VTA by opioids only get worse. It can cause irreversible damage to the central nervous system, hormones, and several other vital functions.

Opioids Neurobiological Effects on Synaptic Plasticity of Locus Coeruleus Neurons

What are Locus Coeruleus Neurons?

Locus coeruleus neurons primarily work to produce wakefulness and alertness. Excited locus coeruleus neurons cause the release of the chemical norepinephrine. Norepinephrine, much like adrenaline, causes increased blood flow, heart rate, and cognitive function.7 The locus coeruleus neurons rely on several brain functions and chemicals to fully function.

How Do Opioids Effect Locus Coeruleus Neurons?

GABA receptors counteract or otherwise inhibits the production of excitable neurons such as locus coeruleus neurons. Opioids stimulate GABA receptors. The result is severely decreased LC neurons, which negatively impacts mental clarity and cognitive performance.8

Morphine’s Effects on Synapses and Pathological Memory

Pathological memory most commonly refers to the loss of memory due to disease or trauma. In the context of synaptic plasticity, it relates to retaining, accessing, or creating new memories.

Morphine severely impairs memory function and even goes so far as to cause amnesia.9 Not all of the changes morphine causes can reverse, and the severity of the changes increases with prolonged morphine use.

Treating the Negative Neuroadaptations of Addiction

Treating negative neuroadaptations of addictions is a two-pronged method involving both treatments and therapies to heal the brain fully. Here are a few of the most common options.

Treatments

IV Amino Acids: Essential amino acids are required for virtually every system in the body. Proper amino acid nutrition results in an improved mood, reduced withdrawal symptoms, and improved cognitive function.10 Intravenous amino acid administration is used to restore amino acids to the body in a medical setting.

Detox: Inpatient detox facilities allow a client 24/7 monitoring while they overcome physical withdrawal of an opioid. Detox offers a safe environment and medical assistance to reduce withdrawal symptoms and cravings.

Buprenorphine: This drug is used to stabilize a person going through withdrawal. Because the brain perceives withdrawal as an inherent negative, reducing the symptoms of withdrawal betters the chance of the brain working towards healing and lowers the chance of relapse.

Therapies

Mindfulness: Mindfulness, a form of meditation, is a practice that helps a client be in more control of their thoughts and cravings. Mindfulness can help build strong coping mechanisms.11

Environmental Changes: Stress heavily contributes to the risk of addiction, and certain environments may further encourage drug use. By separating a client from their potential environmental triggers, they have an opportunity to build healthy coping mechanisms and become aware of their triggers.11

Cognitive Behavioral Therapy: CBT aims to restore healthy behavioral habits. CBT encompasses a broad range of specific therapies all centered around deprogramming substance dependency. In time, a client can expect to better handle stressful situations and gain an improved outlook on life.11

Resources

  1. https://qbi.uq.edu.au/brain-basics/brain/brain-physiology/what-synaptic-plasticity
  2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4046255/
  3. https://www.cdc.gov/drugoverdose/opioids/terms.html#:~:text=%E2%80%9COpiates%E2%80%9D%20vs.,%2C%20semisynthetic%2C%20and%20synthetic%20opioids
  4. https://pubmed.ncbi.nlm.nih.gov/20849328/#:~:text=An%20example%20of%20a%20serotonergic,in%20rats%20and%20nonhuman%20primates
  5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886284/
  6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3002174/
  7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3548657/
  8. https://pubmed.ncbi.nlm.nih.gov/9403690/
  9. https://academic.oup.com/ijnp/article/7/3/311/681894
  10. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4074362/
  11. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5440362/