The retina of the honeybee drone is a nervous tissue in which glial cells and photoreceptor neurons constitute two distinct metabolic compartments. The phosphorylation of glucose and its subsequent incorporation into glycogen occur essentially in glia, whereas O2 consumption occurs in the photoreceptors. After [3H] glucose loading of superfused retinal slices, light stimulation induced a significant rise in [3H] glycogen turnover in the glia. This occurs without a concomitant covalent modification of glycogen enzymes. Probably only an increase or a decrease of the availability of [3H] glycosyls that are incorporated into glycogen is necessary. As only photoreceptors are directly excitable by light, we searched for a signal that stimulates glycogen metabolism in the glia. Although K+ in extracellular space and glia increases after repetitive light stimulation, increasing bath K+ in the dark did not mimic the metabolic effects of light, despite an equivalent increase of K+ in the extracellular space and glia. We subsequently explored the role of cAMP, a universal intracellular second messenger. Exposure of retinal slices to the adenylate-cyclase activator forskolin induced an expected increase in the rate of formation of cAMP, but only partially mimicked the metabolic effects of light. Furthermore, light stimulation failed to induce a rise in the rate of formation of cAMP. We conclude that in this nervous system, without synapses, neither K+ nor cAMP mediates the effect of light stimulation on intraglial glucose metabolism.