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Morphine stimulates nitric oxide release from invertebrate microglia
Y Liu1, D Shenouda, T V Bilfinger
1Neuroscience Research Institute, State University of New York at Old Westbury 11568, USA.
Brain Research
|May 25, 1996
Summary
Morphine stimulates nitric oxide (NO) release in invertebrates, specifically the mussel Mytilus edulis. This finding highlights morphine
Area of Science:
- Neuroscience
- Biochemistry
- Evolutionary Biology
Background:
- Morphine is known to stimulate nitric oxide (NO) release in human endothelial cells.
- The evolutionary conservation of morphine's signaling pathways is not well understood.
Purpose of the Study:
- To investigate whether morphine-induced NO release occurs in invertebrates.
- To determine the role of NO in morphine's effects on microglial egress in the mussel Mytilus edulis.
Main Methods:
- Excised mussel ganglia were exposed to varying doses of morphine.
- Nitric oxide synthase inhibitor (L-NAME) and naloxone were used to assess the mechanisms involved.
- NO release was measured in vitro following morphine stimulation.
Main Results:
- Morphine significantly decreased microglial egress in a dose-dependent and naloxone-sensitive manner.
- Co-incubation with L-NAME reversed the effect of morphine on microglial egress, suggesting NO mediation.
- Morphine stimulated NO release in isolated mussel cells, a process sensitive to naloxone and L-NAME.
Conclusions:
- Morphine stimulates nitric oxide release in invertebrates, conserved across 500 million years of evolution.
- This suggests a fundamental role for morphine as a signaling molecule in diverse animal species.
- The findings underscore the importance of the mu 3 receptor pathway in NO signaling.