M
Michael P. Honchar
Researcher at Washington University in St. Louis
Publications - 7
Citations - 902
Michael P. Honchar is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Lithium (medication) & Pilocarpine. The author has an hindex of 7, co-authored 7 publications receiving 887 citations.
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Journal ArticleDOI
Systemic cholinergic agents induce seizures and brain damage in lithium-treated rats.
TL;DR: Administration of pilocarpine or physostigmine to rats treated with lithium chloride produced sustained limbic seizures, widespread brain damage, and increased concentrations of D-myo-inositol-1-phosphate in the brain.
Journal ArticleDOI
Evidence that Lithium Alters Phosphoinositide Metabolism: Chronic Administration Elevates Primarily d-myo-Inositol-1-Phosphate in Cerebral Cortex of the Rat
TL;DR: Data are presented showing that lithium is an uncompetitive inhibitor of the hydrolysis of both d‐ and l‐M1P by M1P’ase, and evidence that Lithium is largely producing this effect via phospholipase C‐mediated phosphoinositide metabolism is presented.
Journal ArticleDOI
Effects of systemically administered lithium on phosphoinositide metabolism in rat brain, kidney, and testis.
TL;DR: It is believed that these increases in inositol phosphates result from endogenous phosphoinositide metabolism in cerebral cortex and that lithium is capable of modulating that metabolism by reducing cellular myo‐inositol levels.
Journal ArticleDOI
Chronically administered lithium alters neither myo-inositol monophosphatase activity nor phosphoinositide levels in rat brain.
TL;DR: Results are contrary to published reports which suggest that myo‐ inositol monophosphatase activity increases and that the phospha‐tidylinositol level decreases in rat brain as a result of chronic administration of lithium.
Book ChapterDOI
Detection of Receptor-Linked Phosphoinositide Metabolism in Brain of Lithium-Treated Rats
TL;DR: It is believed that the seizure activity itself contributes to the increase in IP observed, which is comparable to the increases obtained with muscarinic agonists but without producing seizures.