scholarly journals Chronic imipramine but not bupropion increases arachidonic acid signaling in rat brain: is this related to ‘switching’ in bipolar disorder?

2008 ◽  
Vol 15 (6) ◽  
pp. 602-614 ◽  
Author(s):  
H-J Lee ◽  
J S Rao ◽  
L Chang ◽  
S I Rapoport ◽  
H-W Kim
Keyword(s):  
Bipolar Disorder ◽  
Arachidonic Acid ◽  
Rat Brain ◽  
Chronic Imipramine

scholarly journals Valnoctamide, which reduces rat brain arachidonic acid turnover, is a potential non-teratogenic valproate substitute to treat bipolar disorder

2017 ◽  
Vol 254 ◽  
pp. 279-283 ◽  
Author(s):  
Hiren R. Modi ◽  
Kaizong Ma ◽  
Lisa Chang ◽  
Mei Chen ◽  
Stanley I. Rapoport
Keyword(s):  
Bipolar Disorder ◽  
Arachidonic Acid ◽  
Rat Brain

Is the brain arachidonic acid cascade a common target of drugs used to manage bipolar disorder?

2009 ◽  
Vol 37 (5) ◽  
pp. 1104-1109 ◽  
Author(s):  
Richard P. Bazinet
Keyword(s):  
Bipolar Disorder ◽  
Valproic Acid ◽  
Arachidonic Acid ◽  
Rat Brain ◽  
Bipolar Depression ◽  
Chronic Administration ◽  
Mood Stabilizers ◽  
Arachidonic Acid Cascade ◽  
Brain Phospholipids ◽  
The Brain

Although lithium has been used therapeutically to treat patients with bipolar disorder for over 50 years, its mechanism of action, as well as that of other drugs used to treat bipolar disorder, is not agreed upon. In the present paper, I review studies in unanaesthetized rats using a neuropharmacological approach, combined with kinetic, biochemical and molecular biology techniques, demonstrating that chronic administration of three commonly used mood stabilizers (lithium, valproic acid and carbamazepine), at therapeutically relevant doses, selectively target the brain arachidonic acid cascade. Upon chronic administration, lithium and carbamazepine decrease the binding activity of activator protein-2 and, in turn, the transcription, translation and activity of its arachidonic acid-selective calcium-dependent phospholipase A2 gene product, whereas chronic valproic acid non-competitively inhibits long-chain acyl-CoA synthetase. The net overlapping effects of the three mood stabilizers are decreased turnover of arachidonic acid, but not of docosahexaenoic acid, in rat brain phospholipids, as well as decreased brain cyclo-oxygenase-2 and prostaglandin E2. As an extension of this theory, drugs that are thought to induce switching to mania, especially when administered during bipolar depression (fluoxetine and imipramine), up-regulate enzymes of the arachidonic acid cascade and turnover of arachidonic acid in rat brain phospholipids. Future basic and clinical studies on the arachidonic acid hypothesis of bipolar disorder are warranted.

scholarly journals Lamotrigine blocks NMDA receptor-initiated arachidonic acid signalling in rat brain: implications for its efficacy in bipolar disorder

2011 ◽  
Vol 15 (07) ◽  
pp. 931-943 ◽  
Author(s):  
Epolia Ramadan ◽  
Mireille Basselin ◽  
Jagadeesh S. Rao ◽  
Lisa Chang ◽  
Mei Chen ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Arachidonic Acid ◽  
Nmda Receptor ◽  
Rat Brain

Arachidonic Acid Induces ARE/Nrf2-Dependent Heme Oxygenase-1 Transcription in Rat Brain Astrocytes

2017 ◽  
Vol 55 (4) ◽  
pp. 3328-3343 ◽  
Author(s):  
Chih-Chung Lin ◽  
Chien-Chung Yang ◽  
Yu-Wen Chen ◽  
Li-Der Hsiao ◽  
Chuen-Mao Yang
Keyword(s):  
Arachidonic Acid ◽  
Rat Brain ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1

Eicosanoids in Rat Brain during Ischemia and Reperfusion—Correlation to DC Depolarization

1990 ◽  
Vol 10 (3) ◽  
pp. 358-364 ◽  
Author(s):  
F. Tegtmeier ◽  
C. Weber ◽  
U. Heister ◽  
I. Haker ◽  
D. Scheller ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Rat Brain ◽  
Direct Current ◽  
Eicosatetraenoic Acid ◽  
Ischemia And Reperfusion ◽  
Ischemic Time ◽  
Isolated Perfused Rat Brain ◽  
Current Potential

The effects of complete ischemia on cerebral arachidonic acid (AA) metabolism were investigated in the isolated perfused rat brain. During 12.5 min of ischemia, AA, 5-hydroxy-6,8,11,14-eicosatetraenoic acid, and 15-hydroxy-5,8,11,13-eicosatetraenoic acid increased 129-, 4-, and 10-fold, respectively, while subsequent reperfusion for 30 min resulted in normalized levels independently of the duration of preceding ischemia. Prostaglandin (PG) F2α, PGE2, PGD2, 6-keto-PGF1α, and thromboxane (Tx) B2 remained at preischemic levels during 12.5 min of complete ischemia. However, at the end of subsequent reperfusion for 30 min, the levels of the prostanoids PGF2α, PGE2, PGD2, 6-keto-PGF1α, and TxB2 increased according to the preceding ischemic time. The levels reached a maximum after 7.5 min of ischemia and were elevated by 7-, 14-, 48-, 3-, and 30-fold, respectively. A prolongation of ischemia of up to 12.5 min was not associated with further increases of prostanoids at the end of reperfusion. The mechanisms underlying the metabolism of eicosanoids are discussed in relation to the changes of cortical direct current potential.

Molecular Characterization of an Arachidonic Acid Epoxygenase in Rat Brain Astrocytes

Stroke ◽  
1996 ◽  
Vol 27 (5) ◽  
pp. 971-979 ◽  
Author(s):  
Nabil J. Alkayed ◽  
Jayashree Narayanan ◽  
Debebe Gebremedhin ◽  
Meetha Medhora ◽  
Richard J. Roman ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Rat Brain ◽  
Molecular Characterization
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