Impaired anandamide/palmitoylethanolamide signaling in hippocampal glutamatergic neurons alters synaptic plasticity, learning, and emotional responses
Laboratory studyOther animals
- Design
- Laboratory study
- Subjects
- Adult mice with FAAH selectively overexpressed in hippocampal CA1-CA3 glutamatergic neurons, using a Cre/loxP and AAV delivery system
- Dose used in the study
- Not applicable; this study manipulated the enzyme (FAAH) that breaks down PEA and anandamide, rather than administering PEA
- Duration
- Not stated in the abstract
- What was measured
- Hippocampal FAAH activity; anandamide, PEA, 2-AG and OEA levels; synaptic activity and long-term potentiation/depression by electrophysiology; anxiety-like behaviour, object recognition memory and fear extinction
What the authors reported
FAAH overexpression raised its enzymatic activity and lowered hippocampal anandamide and PEA (2-AG and OEA unchanged). This increased excitatory and inhibitory synaptic activity and long-term potentiation, without changing long-term depression or short-term plasticity. Behaviourally, it raised anxiety-like behaviour and impaired object recognition memory and fear-memory extinction.
Limits of this study
A genetically modified mouse model; it cannot show effect in people. Funding and conflicts not stated in the abstract.
Source
PubMed 30532004 · doi:10.1038/s41386-018-0274-7
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.