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.