Topical correlation of increased hippocampal glutamine synthetase immunoreactivity and glutamatergic terminal fields after entorhinal cortex lesion

Many astrocyte functions are related to glutamatergic transmission and to o ther synaptic functions, such as glutamate uptake and glutamate metabolism. While many of these functions can be executed by perisynaptic astrocyte pr ocesses, it is not clear how these processes are formed. One of the factors guiding them to the synapse may be synaptically released glutamate. This w ould explain the topical correlation between laminated glutamatergic termin al fields and laminae most intensely labeled by a cytoplasmic astrocyte mar ker, anti-glutamine synthetase (GS). This hypothesis was tested by selectiv ely increasing the glutamate content in one terminal field. The rat entorhi nal cortex, the origin of the glutamatergic projection to the outer molecul ar layer (OML) of the hippocampal fascia dentata, was lesioned electrolytic ally. In line with the hypothesis, GS immunoreactivity was strongly increas ed in the OML at 6 and 8 days postlesion. Lesion of only the medial entorhi nal cortex resulted in heavily increased GS immunoreactivity only in the ce ntral portion of the molecular layer (i.e., the corresponding terminal fiel d). The laminae affected were always separated from neighboring fields by a straight and clear-cut line. Although many other factors are released in t he terminal field after lesion, the results are consistent with a guiding r ole for glutamate. The lamina-specific effect suggests that the factor(s) i nvolved have a very limited diffusion distance. The straight border line be tween affected and unaffected laminae, which cuts across astrocyte territor ies, can best be explained by ramification of only those processes of a giv en astrocyte that are contained within the lamina affected. (C) 2000 Wiley- Liss, Inc.