scholarly journals Time-dependent changes in the brain arachidonic acid cascade during cuprizone-induced demyelination and remyelination

2011 ◽  
Vol 85 (1) ◽  
pp. 29-35 ◽  
Author(s):  
S. Palumbo ◽  
C.D. Toscano ◽  
L. Parente ◽  
R. Weigert ◽  
F. Bosetti
2009 ◽  
Vol 37 (5) ◽  
pp. 1104-1109 ◽  
Author(s):  
Richard P. Bazinet

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.


2020 ◽  
Vol 16 (1) ◽  
pp. 90-93
Author(s):  
Carmen E. Iriarte ◽  
Ian G. Macreadie

Background: Parkinson's Disease results from a loss of dopaminergic neurons, and reduced levels of the neurotransmitter dopamine. Parkinson's Disease treatments involve increasing dopamine levels through administration of L-DOPA, which can cross the blood brain barrier and be converted to dopamine in the brain. The toxicity of dopamine has previously studied but there has been little study of L-DOPA toxicity. Methods: We have compared the toxicity of dopamine and L-DOPA in the yeasts, Saccharomyces cerevisiae and Candida glabrata by cell viability assays, measuring colony forming units. Results: L-DOPA and dopamine caused time-dependent cell killing in Candida glabrata while only dopamine caused such effects in Saccharomyces cerevisiae. The toxicity of L-DOPA is much lower than dopamine. Conclusion: Candida glabrata exhibits high sensitivity to L-DOPA and may have advantages for studying the cytotoxicity of L-DOPA.


2005 ◽  
Vol 69 (3) ◽  
pp. 107-127 ◽  
Author(s):  
Natalia V. Bogatcheva ◽  
Marina G. Sergeeva ◽  
Steven M. Dudek ◽  
Alexander D. Verin

1986 ◽  
Vol 40 ◽  
pp. 233
Author(s):  
Ryota Yoshimoto ◽  
Toshihiko Ishimitsu ◽  
Yoshikatsu Koyama ◽  
Shigebumi Hashimoto ◽  
Hiroaki Matsuoka ◽  
...  

2008 ◽  
Vol 138 (12) ◽  
pp. 2515-2520 ◽  
Author(s):  
Stanley I. Rapoport
Keyword(s):  

Sign in / Sign up

Export Citation Format

Share Document