Significance of the potassium signal from neurones to glial cells

Abstract

Neurones transmit signals to glial cells by releasing potassium into the intercellular spaces during nerve activity, simultaneously depolarizing their membrane potential¹. It is thought that the glial cells may respond metabolically or trophically to the released K, and that they may also take up excess K, thereby protecting the neurones against perturbations in the extracellular concentration of this ion^2,3. We have studied metabolic interactions between the two cell types in leech and snail ganglia using a recently discovered application^4,5 of the radioactively labelled 2-deoxyglucose (2-DG) technique⁶. This approach derives from the finding that ³H-2-DG is partially and selectively metabolized into glycogen within nervous tissue, and thus can be used as a sensitive, specific marker for mapping sites of glycogen synthesis and distribution in nervous tissue^4,5. In the leech and snail ganglia, the large size of the neuronal perikarya, together with the grouping of the glial cells around them and the location of the axonal and dendritic processes in the core of the ganglia, allows the distributions of the labelled glycogen in the different cell types and their processes to be resolved by light and electron microscope autoradiography^7,8. Here we describe how in both animals, antidromic stimulation of nerves entering the ganglia increased the incorporation of ³H-2-DG into glycogen in glial cells surrounding the activated neurones. Increased extracellular K had a similar effect, which was maximal for a K concentration ∼4mM above normal. We therefore conclude that neuronal activation causes a K-mediated increase in ³H-2-DG uptake and synthesis into glycogen by the satellite glial cells.