Carbachol- and KCl-induced changes in phosphoinositide metabolism and free calcium in guinea pig cerebral cortex synaptosomes

  title={Carbachol- and KCl-induced changes in phosphoinositide metabolism and free calcium in guinea pig cerebral cortex synaptosomes},
  author={M-R. Hirvonen and Hannu Komulainen and Kai M. Savolainen},
  journal={Neurochemical Research},
Phosphoinositide (PI) and calcium metabolism were studied in guinea pig cerebral cortex synaptosomes. Mass amounts of inositol and inositol monophosphates, and the levels of free intrasynaptosomal calcium ([Ca2+]i) were measured after KCl (60 mM), after a direct cholinergic agonist carbachol (CA, 1mM), and after their combination. Inositol, inositol-1-phosphate (Ins1P), inositol-4-phosphate (Ins4P) and [Ca2+]i were measured with and without 10 mM LiCl in the incubation medium. CA-induced… 


Membrane depolarization and carbamoylcholine stimulate phosphatidylinositol turnover in intact nerve terminals.
Data show that both Ca2+ influx and M1 muscarinic receptor activation stimulate phospholipase C activity in synaptosomes, suggesting that phosphatidylinositol turnover may be involved in regulating neurotransmitter release from nerve terminals.
Is Inositol Bisphosphate the Product of A23187 and Carbachol‐Mediated Polyphosphoinositide Breakdown in Synaptosomes?
There was no detectable accumulation of inositol trisphosphate in the presence of carbachol, K+, orcarbachol plus K+, even after short (30 s.) incubations, and this does not appear to result from rapid formation ofInositol tetrakisph phosphate or from enhanced breakdown of the tr isphosphates in synaptosomes.
Kinetic Analysis of A23187‐Mediated Polyphosphoinositide Breakdown in Rat Cortical Synaptosomes Suggests that Inositol Bisphosphate Does Not Arise Primarily by Degradation of Inositol Trisphosphate
Analysis of 32P‐labelled synaptosomes reveals that A23187 produces Ca2+‐dependent losses of PtdInsP2, PtdlnsP, ATP, and GTP radioactivity and a marked increase in the radioactivity of a compound distinct from nucleotides or any of the lipid breakdown products tested.
Cerebral lithium, inositol and inositol monophosphates.
  • M. Hirvonen
  • Biology, Medicine
    Pharmacology & toxicology
  • 1991
Lithium-induced accumulation of Ins1P or changes of Ins4P levels do not explain lithium-induced decrease in cerebral inositol, and effects of lithium on brain P1 turnover are likely to be multifocal and to differ markedly at different concentrations of Li+ in the brain.
Effects of lithium on synaptosomal Ca2 + fluxes
The results suggest that lithium does not directly interact with synaptosomal Ca2 + flux, but rather may influence Ca 2 + flux through an indirect mechanism following chronic treatment.
The effects of lithium ion and other agents on the activity of myo-inositol-1-phosphatase from bovine brain.
Changes in cerebral inositol-1-phosphate concentrations in LiCl-treated rats: Regional and strain differences
LiCl-induced (5 mEq/kg) regional differences in the cerebral phosphoinositide (PI) cycle were studied by measuring inositol-1-phosphate (Ins-1-P), an, intermediate in the PI cycle, in male Sprague