title: Metabolite changes in the cerebral cortex of treated and untreated infant hydrocephalic rats studied using in vitro 31P-NMR spectroscopy.
abstract: The effect of hydrocephalus on cerebral energy metabolites and on intermediates of membrane phospholipid metabolism has been studied in H-Tx rats with inherited infantile hydrocephalus. Hydrocephalic rats and rats with shunts placed at 4-5 days or at 10 days after birth were subjected to magnetic resonance imaging in vivo before 21 days of age to determine the dimensions of the ventricles and cortex. At 21 days, the brains from the three groups of rats, together with age-matched control littermates, were frozen in situ, and chloroform/methanol extracts of cerebral cortex were prepared for high-resolution 31P-NMR spectroscopy. Hydrocephalus resulted in modest decreases in most metabolites quantified. Levels of phosphocreatine, ATP, and diphosphodiesters plus NAD were significantly reduced by 23-32%, and inorganic phosphate content was reduced but not significantly. Levels of the membrane phospholipid intermediates phosphorylethanolamine, glycerophosphorylethanolamine, and glycerophosphorylcholine were also significantly reduced by 30-33%, indicating changes in membrane metabolism. These general decreases are consistent with a loss of cell contents, possibly due to changes in dendrite structure in hydrocephalus. Rats shunt-treated at 4-5 days were similar to control rats for all energy metabolites, but those treated later at 10 days had reduced phosphocreatine and ATP levels. Shunt-treated rats also had reductions in levels of membrane phospholipids, some of which occurred in sham-operated rats. It is concluded that hydrocephalus leads to reductions in levels of energy metabolites and in levels of membrane phospholipids and that the changes in energy metabolites can be reversed by early, but not by later, shunt treatment.
authors.affiliation: Department of Pharmacology, University of Florida, Gainesville 32610, USA.
authors.forename: N G
authors.initials: NG
authors.lastname: Harris
authors.forename: H D
authors.initials: HD
authors.lastname: Plant
authors.forename: R W
authors.initials: RW
authors.lastname: Briggs
authors.forename: H C
authors.initials: HC
authors.lastname: Jones
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology; D002552:Cerebral Ventricles / Q000378:metabolism / Q000473:pathology; D002557:Cerebrospinal Fluid Shunts; D004734:Energy Metabolism; D006849:Hydrocephalus / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D008563:Membrane Lipids / Q000378:metabolism; D009243:NAD / Q000378:metabolism; D010710:Phosphates / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D010743:Phospholipids / Q000378:metabolism; D010758:Phosphorus; D051381:Rats; D011922:Rats, Mutant Strains; D012016:Reference Values
chemical_list: D008563:Membrane Lipids; D010710:Phosphates; D010743:Phospholipids; D010725:Phosphocreatine; D009243:NAD; D010758:Phosphorus; D000255:Adenosine Triphosphate