A new method of measurement of the concentration of brain glycogen has been developed. Following stab wound in brain, cyclic AMP was found to increase, phosphorylase a was activated, and there was an initial decrease in glycogen. Subsequently, glycogen synthase was activated and glycogen in the injured brain increased 3-4 fold greater than in control brain. The results following drug treatments indicate that the cyclic AMP increase may be mediated by adenosine, rather than inhibition of phosphodiesterase, or activation of adenyl cyclase by other mediators such as norepinephrine. Further work is planned to determine the regulation of glycogen turnover in C-6 astrocytoma and C-1300 neuroblastoma cells in culture.