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Main Title Age-Dependent Changes in Receptor-Stimulated Phosphoinositide Turnover in the Rat Hippocampus.
Author Tandon, P. ; Mundy, W. R. ; Ali, S. F. ; Nanry, K. ; Rogers, B. C. ;
CORP Author National Inst. of Environmental Health Sciences, Research Triangle Park, NC. Lab. of Molecular and Integrative Neuroscience. ;National Center for Toxicological Research, Jefferson, AR. Div. of Reproductive and Developmental Toxicology.;Health Effects Research Lab., Research Triangle Park, NC.
Publisher c1991
Year Published 1991
Report Number EPA/600/J-92/253;
Stock Number PB92-206333
Additional Subjects Aging(Biology) ; Hippocampus ; Phosphoinositides ; Cholinergic receptors ; Learning ; Rats ; Muscarinic receptors ; Choline acetyltransferase ; Ion exchange chromatography ; Reprints ;
Library Call Number Additional Info Location Last
NTIS  PB92-206333 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 9p
To study the changes in the hippocampal cholinergic system of chronologically old and behaviorally impaired animals, old (21 months of age) and young (3 months of age) male, Fischer-344 rats were used. The aged animals were tested on a reference memory task (Morris water maze) and found to be functionally impaired as compared to the young controls. Carbachol-stimulated phosphoinositide metabolism was measured in hippocampal slices from young and old rats. Slices were prelabeled with (3)H-inositol for 120 min and subjected to muscarinic stimulation in the presence of lithium. Following extraction of the slices with acidified solvent mixture, the inositolphosphates present in the aqueous fraction were isolated by ion exchange chromatography. Receptor-stimulated release of inositolphosphates (IPs) was found to be increased in the hippocampus of older animals. The age-related enhancement of IP release was in contrast to the decrease in choline acetyltransferase (CHAT) activity in the hippocampus. The authors postulate that alterations in the G-protein coupling with the muscarinic receptor leads to an increase in the phosphoinositide turnover in part as a compensatory mechanism for neuronal cell death and reduced transmitter levels.