Ultra-micronized palmitoylethanolamide rescues the cognitive decline-associated loss of neural plasticity in the neuropathic mouse entorhinal cortex-dentate gyrus pathway
Laboratory studyOther animals
- Design
- Laboratory study
- Subjects
- Mice with spared nerve injury (SNI) of the sciatic nerve, and PPARalpha-null mice
- Dose used in the study
- Not stated in the abstract
- Duration
- Chronic treatment starting once neuropathic pain was fully developed; exact duration not stated
- What was measured
- Mechanical and thermal pain thresholds, spatial memory, long-term potentiation (LTP) at the entorhinal cortex-dentate gyrus pathway, and glutamatergic synapse markers
What the authors reported
Nerve injury reduced pain thresholds, spatial memory and LTP, altered dentate gyrus synapse structure and glutamate receptor expression, and raised glutamate and 2-AG levels. Chronic PEA reversed the pain, memory and LTP deficits and restored synaptic changes in wild-type mice, but not in PPARalpha-null mice.
Limits of this study
A mouse model of nerve-injury pain; it cannot show effect in people. Funding and conflicts not stated in the abstract.
Source
PubMed 30266286 · doi:10.1016/j.nbd.2018.09.023
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.