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Related Experiment Video

Updated: Jun 17, 2026

Lipidomics and Transcriptomics in Neurological Diseases

Lipidomics and Transcriptomics in Neurological Diseases

Published on: March 18, 2022

Mood-stabilizers target the brain arachidonic acid cascade.

Jagadeesh S Rao¹, Stanley I Rapoport

¹Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA. jrao@mail.nih.gov

Current Molecular Pharmacology

|December 22, 2009

Summary

Mood stabilizers for bipolar disorder (BD) reduce arachidonic acid (AA) signaling in rat brains. Targeting AA pathways may offer new treatments for this severe psychiatric illness.

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Published on: January 3, 2017

Area of Science:

Neuroscience
Psychiatry
Pharmacology

Background:

Bipolar disorder (BD) is a severe psychiatric illness with recurrent manic and depressive episodes.
The exact neuropathology and etiology of BD remain unclear, despite effective treatments targeting various signaling pathways.

Purpose of the Study:

To investigate the mechanisms of action of mood stabilizers in the context of BD.
To explore the role of the arachidonic acid (AA) cascade in BD and its potential as a therapeutic target.

Main Methods:

Review of studies on mood stabilizers (lithium, carbamazepine, valproate, lamotrigine) in rat models of BD.
Analysis of effects on cytosolic phospholipase A(2) (cPLA(2)), cyclooxygenase-2 (COX-2), and their transcription factors (AP-2, NF-kappaB).
Examination of AA turnover in brain phospholipids.

Main Results:

Mood stabilizers effective in BD decreased the transcription of cPLA(2) and COX-2 and reduced levels of AP-2 and NF-kappaB in rat brains.
Anti-manic drugs decreased arachidonic acid (AA) turnover in brain phospholipids with chronic administration.
These findings suggest that effective BD treatments commonly target AA cascade enzymes and their transcription factors.

Conclusions:

Bipolar disorder is potentially associated with increased brain AA signaling.
Developing therapeutic agents that suppress brain AA signaling could provide novel treatment options for BD.
Further research into mood stabilizer mechanisms and docosahexaenoic acid's effects on AA cascade enzymes is warranted for BD.