Abstract
Opioid addiction is a condition of the central nervous system that occurs as a result of using opiate-based substances, which can be either natural or synthetic chemicals. These have effects identical to those of morphine and work by interacting with opioid receptors such as morphine, heroin, opium, buprenorphine, and Oxycontin. Dopamine has been suggested to play a role in the mechanisms linked to opioid addiction. Additionally, neurotransmitters such as serotonin, norepinephrine, glutamate, and GABA may also have a significant impact. These processes play a critical role in the formation of brain circuits that are involved in the development of addictive behavior. The PI3K-Akt-mTOR pathway is widely recognized as an essential regulator of the effects induced by neurotransmitters on synaptic plasticity, protein synthesis, and cellular responses. This interplay has considerable importance in the development and persistence of opioid addiction, impacting several domains, including reward processing, stress reactivity, and brain plasticity. The understanding of these neurochemical modifications provides vital insights into the underlying mechanisms of addiction and presents potential pathways for treatments. The review enlisted the clinical trials of different types of opioid addiction or dependence. The review offers a succinct summary of many studies that establish a correlation between the PI3K/Akt-mTOR signaling pathway and various receptors implicated in multiple forms of opioid-related dependency.
| Original language | English |
|---|---|
| Pages (from-to) | 652-668 |
| Number of pages | 17 |
| Journal | CNS and Neurological Disorders - Drug Targets |
| Volume | 24 |
| Issue number | 9 |
| DOIs | |
| State | Published - 2025 |
| Externally published | Yes |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- GABA
- Opioid dependence
- PI3K-Akt-mTOR
- dopamine
- inflammation
- neurotransmitters
- oxidative stress
- serotonin
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