alpha-Methyl-p-tyrosine inhibits the production of free arachidonic acid and diacylglycerols in brain after a single electroconvulsive shock.

A single electroconvulsive shock (ECS) significantly enlarged the free fatty acid (FFA) pool of the mouse brain, arachidonic acid being the most actively released FFA (48% over controls). In animals pretreated with alpha-methyl-p-tyrosine (alpha-MT), the endogenous levels of FFA (25 sec after decapitation) were decreased and the effect of ECS was completely abolished. The most pronounced inhibition took place in free arachidonic acid (42% and 52% under controls in nonstimulated and ECS-stimulated mice, respectively). A similar tendency, although lower and less specific than the one taking place in FFA, was observed in mouse brain diacylglycerols (DG). In contrast to ECS, alpha-MT treatment did not effect the marked release of FFA and DG taking place 3 min after decapitation. Taking into account the specific inhibitory action of alpha-MT on tyrosine hydroxylase activity, the present findings provide experimental in vivo evidence about the relationship between biogenic amines and membrane lipid breakdown during electrical stimulation and suggest an involvement of FFA and DG in neurotransmission.