N-palmitoylethanolamine modulates hippocampal neuroplasticity in rats with stress-induced depressive behavior phenotype
Laboratory studyOther animals
- Design
- Laboratory study
- Subjects
- Rats exposed to unpredictable chronic mild stress, and HT22 mouse hippocampal cells treated with corticosterone
- Dose used in the study
- Not stated in the abstract
- Duration
- Not stated in the abstract
- What was measured
- Depression-like behaviour, hippocampal neurogenesis (BrdU, NeuN), synaptic proteins (NCAM, MAP2, SYN, PSD95), and neuronal apoptosis markers, with and without the PPAR-alpha antagonist MK886
What the authors reported
PEA improved the depression-like phenotype, prevented the stress-induced fall in BrdU-positive cells, increased BrdU/NeuN co-localisation and raised synaptic protein levels in the hippocampus. In HT22 cells PEA reduced corticosterone-induced neuron loss, lowered caspase-3 and raised the Bcl-2/Bax ratio. MK886 partly or fully reversed these effects.
Limits of this study
A rat and cell study; it cannot show effect in people. Doses, route, group sizes and treatment length are not in the abstract. The authors declare no competing interests.
Source
PubMed 37673363 · doi:10.1016/j.ejphar.2023.176041
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.