Where it comes from
- Made in
- Adrenal medulla and the brain’s enkephalin neurons
- Sent out by
- With the enkephalins and catecholamines
- Acts on
- Opioid receptors in spinal cord and brainstem
What it does
- An opioid agonist in its own right, present in the brain of rat, cattle and man at levels close to met-enkephalin’s 1
- Lasts longer than the pentapeptide, and its Arg-Phe ending also resembles the RF-amide peptides
- Trimmed back to met-enkephalin by peptidases, which is why its own actions are hard to isolate 1
In medicine
- No medicine copies it or blocks it, and no clinical laboratory measures it
- It has been measured in people in research: low-frequency electrical nerve stimulation raised it in lumbar spinal fluid while high-frequency stimulation raised dynorphin A instead, the clearest human evidence that the two opioid systems are recruited separately 3
Beyond the body’s own use
- Nothing is in trials. The peptide is a laboratory reagent, used mostly in binding experiments, and no analogue of it has been given to a person
- Which receptor it prefers is unsettled and may differ between species: work in frog and rat brain put it at kappa and delta sites, while binding in human cerebral cortex found high affinity at mu and almost none at delta or kappa 2
- What is unresolved is how much of its effect is its own. Peptidases take the Arg-Phe off and leave met-enkephalin, so an experiment that gives MERF becomes, within minutes, an experiment that gives met-enkephalin 1
Sources
- Rossier et al., Met-enkephalin-Arg-Phe, present in high amounts in brain, is an opioid agonist, Nature 1980
- Kim et al., Receptor selectivity of Met-enkephalin-Arg-Phe in human and rat cerebral cortex, Life Sciences 2000
- Han et al., Effect of low- and high-frequency nerve stimulation on Met-enkephalin-Arg-Phe and dynorphin A in human lumbar CSF, Pain 1991
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.