These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: A comparison of lithium effects on human brain and rat brain noradrenaline-sensitive adenylate cyclase. Author: Klein E, Belmaker RH, Newman M, Gruszkiewicz J. Journal: Acta Pharmacol Toxicol (Copenh); 1985; 56 Suppl 1():15-20. PubMed ID: 2984883. Abstract: Lithium (Li) is a drug with numerous biochemical effects. Many of these biochemical effects occur only at high Li concentrations, or disappear after chronic Li treatment. Such effects are probably not related to Li's mechanism of therapeutic action. Inhibition of noradrenaline (NE)-sensitive adenylate cyclase has been proposed as a possible therapeutic mechanism of action for Li. Tolerance does not develop to this effect, which has been reported to occur reliably beginning at 2mM Li in rat cortex. Since 2mM Li is at the upper limit of therapeutic levels in humans, controversy has continued as to whether Li inhibition of NE-sensitive adenylate cyclase is a mechanism of Li's therapeutic action or a mechanism of Li toxicity. We hypothesized that human brain NE-sensitive adenylate cyclase may be more sensitive to Li inhibition than rat brain NE-sensitive adenylate cyclase. Fresh cortical human grey matter was obtained from the edges of surgically removed brain tumors in seven patients. Results showed significant inhibition of NE-sensitive adenylate cyclase at 1mM Li. These results support the possibility that inhibition of NE-sensitive adenylate cyclase is a mechanism of Li's therapeutic action.[Abstract] [Full Text] [Related] [New Search]