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

Abstract

Many astrocyte functions are related to glutamatergic transmission and to other synaptic functions, such as glutamate uptake and glutamate metabolism. While many of these functions can be executed by perisynaptic astrocyte processes, it is not clear how these processes are formed. One of the factors guiding them to the synapse may be synaptically released glutamate. This would explain the topical correlation between laminated glutamatergic terminal fields and laminae most intensely labeled by a cytoplasmic astrocyte marker, anti-glutamine synthetase (GS). This hypothesis was tested by selectively increasing the glutamate content in one terminal field. The rat entorhinal cortex, the origin of the glutamatergic projection to the outer molecular layer (OML) of the hippocampal fascia dentata, was lesioned electrolytically. In line with the hypothesis, GS immunoreactivity was strongly increased in the OML at 6 and 8 days postlesion. Lesion of only the medial entorhinal cortex resulted in heavily increased GS immunoreactivity only in the central portion of the molecular layer (i.e., the corresponding terminal field). The laminae affected were always separated from neighboring fields by a straight and clear-cut line. Although many other factors are released in the terminal field after lesion, the results are consistent with a guiding role for glutamate. The lamina-specific effect suggests that the factor(s) involved have a very limited diffusion distance. The straight border line between affected and unaffected laminae, which cuts across astrocyte territories, can best be explained by ramification of only those processes of a given astrocyte that are contained within the lamina affected.