Beta-adrenergic coupled phospholipid methylation. A possible role in withdrawal from chronic ethanol

Abstract

Phospholipid methylation was studied in rat brain cortex preparations. Adrenergic agonists stimulated methylation in a dose-dependent manner. The effect was stereospecific and the order of potency of agonists was isoproterenol greater than norepinephrine greater than or equal to epinephrine. The stimulation could be blocked by propranolol. It was concluded that adrenergic stimulation of phospholipid methylation in these preparations involved a beta-adrenergic receptor and that this response was dependent upon an intact membrane environment. Neither adenosine nor histamine stimulated methylation. In fact, histamine appeared to inhibit methylation. Cleavage of phosphatidylcholine to lyso-phosphatidylcholine occurred in the presence of either adrenergic agonists or histamine, indicating an involvement of phospholipase A2. Norepinephrine-sensitive methylation in cortex homogenates from rats withdrawn from chronic ethanol administration was double that of controls by 72 hr after the final ethanol dose. Furthermore, basal methylation exhibited a decreasing trend during this period.