Summary of OPRM1
The OPRM1 gene codes for the mu opioid receptor. This receptor is activated by your body’s natural opioids (such as beta-endorphins) and by opioid medications (such as morphine) [R].
OPRM1 promotes pain relief. OPRM1 activation also leads to the release of dopamine, a chemical messenger that promotes feelings of pleasure. This process is involved in reward-seeking and addictive behaviors [R, R, R].
OPRM1 variants have been linked to opioid addiction and heavy alcohol intake [R, R, R, R].
Protein names
Recommended name:
Mu-type opioid receptorShort name:
MOPAlternative name(s):
M-OR-1MOR-1
Mu opiate receptor
Mu opioid receptor
hMOP
- RS10485057 (OPRM1) ??
- RS1799971 (OPRM1) ??
- RS1799972 (OPRM1) ??
- RS2075572 (OPRM1) ??
- RS2236256 (OPRM1) ??
- RS3778151 (OPRM1) ??
- RS3823010 (OPRM1) ??
- RS495491 (OPRM1) ??
- RS538174 (OPRM1) ??
- RS540825 (OPRM1) ??
- RS563649 (OPRM1) ??
- RS609148 (OPRM1) ??
- RS675026 (OPRM1) ??
- RS9384179 (OPRM1) ??
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Top Gene-Substance Interactions
OPRM1 Interacts with These Diseases
| Disease | Score |
Fixes
Natural Ways to Increase Opioid Activity
All of these give us a positive feeling, and at least some of it is because of the opioid system in our body. The following either increase activation of our mu opioid receptors, increase endorphins, which naturally activate our mu-opioid receptors, or make our receptors more sensitive.
Substances That Increase OPRM1
| Substances | Interaction | Organism | Category |
Substances That Decrease OPRM1
| Substances | Interaction | Organism | Category |
Advanced Summary
Activation of the mu receptor by a substance such as morphine causes sedation, euphoria and decreased respiration (R). Although morphine increases sedation, it decreases the total amount of deep sleep and rapid eye movement sleep in humans. (R).
Individual differences in the function of the mu-receptor system predict personality traits that confer vulnerability to or resiliency against risky behaviors such as the predisposition to develop substance use disorders (R).
Activating opioid receptors promote eating and weight gain, at least in the short term (R). When fed a high-fat diet, mice without mu-opioid receptors were resistant to obesity, despite having similar calorie intake to normal mice fed a high-fat diet. This resistance to obesity with the mutant mouse without mu-opioid receptors was associated with increased fatty acid oxidation within muscles (R).
When food proteins are digested, they produce peptides that block mu-opioid activity. These peptides are released in the vein that brings blood flow to the gut.
The vagus nerves communicate with the brain initiate satiety as a result of the mu-opioid blocking (as a result of sensing gut gluconeogenesis) (R). This is one reason why a protein rich diet aids in weight loss.
When the mice were switched from a starch- to a protein-enriched diet, mice reduced their food intake by about 20%, but no such effect occurred in the mice lacking the mu-opioid receptors (R).
Conditions with Increased Gene Activity
| Condition | Change (log2fold) | Comparison | Species | Experimental variables | Experiment name |
|---|
Conditions with Decreased Gene Activity
| Condition | Change (log2fold) | Comparison | Species | Experimental variables | Experiment name |
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Technical
The following transcription factors affect gene expression:
Tissue specificity:
Expressed in brain. Isoform 16 and isoform 17 are detected in brain.
Gene Pathways:
Molecular Function:
- Beta-Endorphin Receptor Activity
- G-Protein Alpha-Subunit Binding
- G-Protein Beta-Subunit Binding
- G-Protein Coupled Receptor Activity
- Morphine Receptor Activity
- Neuropeptide Binding
- Voltage-Gated Calcium Channel Activity
Biological Processes:
- Acute Inflammatory Response To Antigenic Stimulus
- Adenylate Cyclase-Activating Dopamine Receptor Signaling Pathway
- Adenylate Cyclase-Inhibiting Opioid Receptor Signaling Pathway
- Behavioral Response To Ethanol
- Cellular Response To Morphine
- Cellular Response To Stress
- Chemical Synaptic Transmission
- Eating Behavior
- Estrous Cycle
- Excitatory Postsynaptic Potential
- G-Protein Coupled Receptor Signaling Pathway, Coupled To Cyclic Nucleotide Second Messenger
- Locomotory Behavior
- Negative Regulation Of Adenylate Cyclase Activity
- Negative Regulation Of Camp-Mediated Signaling
- Negative Regulation Of Cell Proliferation
- Negative Regulation Of Cytosolic Calcium Ion Concentration
- Negative Regulation Of Nitric Oxide Biosynthetic Process
- Negative Regulation Of Wnt Protein Secretion
- Phospholipase C-Activating G-Protein Coupled Receptor Signaling Pathway
- Positive Regulation Of Appetite
- Positive Regulation Of Camp-Mediated Signaling
- Positive Regulation Of Cytosolic Calcium Ion Concentration
- Positive Regulation Of Erk1 And Erk2 Cascade
- Positive Regulation Of Neurogenesis
- Positive Regulation Of Nitric Oxide Biosynthetic Process
- Regulation Of N-Methyl-D-Aspartate Selective Glutamate Receptor Activity
- Regulation Of Sensory Perception Of Pain
- Response To Cocaine
- Response To Food
- Response To Growth Factor
- Response To Lipopolysaccharide
- Response To Radiation
- Sensory Perception
- Sensory Perception Of Pain
- Wound Healing
Drug Bank:
- Levomethadyl Acetate
- Alvimopan
- Amitriptyline
- Anileridine
- Butorphanol
- Codeine
- Dextromethorphan
- Dextropropoxyphene
- Dezocine
- Diphenoxylate
- Ethylmorphine
- Fentanyl
- Heroin
- Hydrocodone
- Hydromorphone
- Ketamine
- Levallorphan
- Levorphanol
- Loperamide
- Methadone
- Methadyl Acetate
- Pethidine
- Naloxegol
- Naloxone
- Naltrexone
- Ondansetron
- Oxymorphone
- Pentazocine
- Remifentanil
- Sufentanil
- Tapentadol
- Methylnaltrexone
- Alfentanil
- Buprenorphine
- Eluxadoline
- Ketobemidone
- Morphine
- Nalbuphine
- Oxycodone
- Tramadol