Modulation of phospholipid methylation in rat striatum by the corticostriatal pathway.
Surgical undercutting of cortical afferents and subsequent interruption of excitatory input increased phospholipid (PL) methylation (30-40%) in rat striatal synaptosomes as early as 3 days after lesion. The increase was still present 60 days after lesion, was protein-dependent and lesion-specific. The role of the dopaminergic agents on PL methylation in decorticated rats was investigated. In contrast with sham-lesioned rats, in which dopamine stimulated PL methylation, dopamine did not further stimulate phosphatidylethanolamine N-methyltransferase (PEMT) activity in decorticated rats. In addition, dopamine antagonists reversed the increase in PL methylation in lesioned rats at concentrations that had no effect in blocking DA-stimulated PL methylation in sham-lesioned rats. The specific antagonist of N-methyl-D-aspartate receptors, 2-amino-5-phosphonovaleric acid, increased PL methylation in non-lesioned striata, mimicking the effect of decortication, while N-methyl-D-aspartic acid counteracted the decortication-induced increase in PEMT activity. These data suggest a modulatory role of the cortex on PEMT activity in rat striatum.
Tacconi
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Laboratory for Enzyme Research, Istituto di Ricerche Farmacologiche, Mario Negri, Milan, Italy.
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D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D002540:Cerebral Cortex / Q000502:physiology*; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D004298:Dopamine / Q000494:pharmacology; D005260:Female; D005971:Glutamates / Q000378:metabolism; D006220:Haloperidol / Q000494:pharmacology; D007700:Kinetics; D008745:Methylation; D016202:N-Methylaspartate; D010743:Phospholipids / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values
D005971:Glutamates; D010743:Phospholipids; D001224:Aspartic Acid; D016202:N-Methylaspartate; D006220:Haloperidol; D004298:Dopamine