Palmitoylethanolamide inhibits glutamate release in rat cerebrocortical nerve terminals
Laboratory studyOther animals
- Design
- Laboratory study
- Subjects
- Isolated nerve terminals (synaptosomes) from rat cerebral cortex
- Dose used in the study
- PEA applied directly to the synaptosome preparation, at varying concentrations
- Duration
- Not applicable (acute in vitro exposure)
- What was measured
- Calcium-dependent glutamate release triggered by a potassium channel blocker, cytosolic calcium levels, and the effect of channel and receptor blockers on PEA's action
What the authors reported
PEA reduced calcium-dependent glutamate release from cortical nerve terminals in a concentration-dependent way, alongside a fall in cytosolic calcium. This effect was blocked by a P/Q-type calcium channel blocker and a protein kinase A inhibitor, and partly blocked by a CB1 receptor antagonist, but was unaffected by two other calcium-release inhibitors.
Limits of this study
An in vitro study using isolated rat nerve terminals; it cannot show effect in the intact brain or in people. Funding and conflicts not stated in the abstract.
Source
PubMed 25768340 · doi:10.3390/ijms16035555
Entry checked against the abstract on PubMed on 2026-09-22. The dose shown is the dose the researchers used. It is not a recommendation. How to read this page.