An increase in GABA-ergic activity has been implicated in the initiation of quasi-morphine abstinence behavior by di-n-propylacetate (DPA). Two structural analogues of DPA, namely, the branched-chain-fatty acid 2-methyl, 2-ethylcaproic acid and 2,2-dimethylvaleric acid have now been used to study this relationship between behavioral and biochemical effects. A correlation appeared to exist between the K1 of these compounds for succinic semi-aldehyde dehydrogenase, the second enzyme in the degradation of GABA, and the doses exerting a maximum effect on behavior. On the other hand concurrent inhibition of GABA-transaminase seemed to suppress the behavioral effects of the fatty acids. This apparent paradox can possibly be explained by supposing a different action of the fatty acids in distinct compartments of the brain, suggesting an important role for increased GABA-ergic activity in the neuronal compartment in the initiation of the quasi-morphine abstinence behavior.
