High-dose intrathecal morphine produced anti-analgesia (pain) through spinal dynorphin release and NMDA receptor activation — the same mechanism as high-dose endomorphin-2, explaining opioid-induced hyperalgesia across opioid classes.
Key findingHigh-dose IT morphine produced anti-analgesia mediated by spinal dynorphin release and NMDA receptor activation (blocked by MK-801 and anti-dynorphin)
What the researchers found
High-dose IT morphine produced anti-analgesia mediated by spinal dynorphin release and NMDA receptor activation (blocked by MK-801 and anti-dynorphin), demonstrating a universal opioid-induced hyperalgesia mechanism across both synthetic and endogenous opioids.
Why it matters
Relevant for opioid-peptides, pain, receptor-signaling.
How the study worked
animal-study study on opioid-peptides, pain.
What this study cannot tell us
See abstract.
How to read the evidence
preliminary evidence.
When this study was published
Published in 2004.
The bigger picture
Advances peptide/biomarker research with clinical implications.
Questions still open
- Further research needed.
- Clinical translation to evaluate.
Common questions
What was studied?
What was found?
Read the original research
Nonopioidergic mechanism mediating morphine-induced antianalgesia in the mouse spinal cord.
The Journal of pharmacology and experimental therapeutics, 310(1), 240-6
Citation
Wu, Hsiang-En; Thompson, Jonathan; Sun, Han-Sen; Leitermann, Randy J; Fujimoto, James M; Tseng, Leon F. (2004). Nonopioidergic mechanism mediating morphine-induced antianalgesia in the mouse spinal cord.. The Journal of pharmacology and experimental therapeutics, 310(1), 240-6.