Intramuscular administration of methionine to mice resulted in changes in the levels of aspartate, glutamate, glutamine, and gamma-aminobutyrate in both nerve endings (synaptosomes) and "non-nerve-ending" tissue in the brain. However, the amino acid changes in the two locations differed considerably, not only in the time to onset of the changes, but also in the direction of the changes and in their duration. The results provide additional support for a glutamate-glutamine cycle between neurons and glia, and suggest that the decreases in amino acid levels in the nerve endings are due to an insufficient supply of glutamine from glia or other cellular structures, possibly compounded by an impairment in the uptake of glutamine into the nerve terminals. The primary cause of the glutamine deficiency is unknown because methionine did not affect the enzymes of glutamate and glutamine metabolism. Treatment of mice with methionine also resulted in an anticonvulsant action, but no correlation was observed between the latter phenomenon and the glutamate content of nerve endings.