IS GLUTAMATE A COTRANSMITTER IN CORTICAL CHOLINERGIC TERMINALS - EFFECTS OF NUCLEUS BASALIS LESION AND OF PRESYNAPTIC MUSCARINIC AGENTS

To obtain additional evidence in support of the co-transmitter role of glutamate in cortical terminals proposed by Docherty et al.8, the right nucleus basalis in rats was lesioned with ibotenic acid; resulting changes in cortical acetycholinesterase (AChE) staining, glutamate content, and the release of [3H]acetylcholine ([3H]ACh) and glutamate from cortical slices from the two sides were compared. While there was a profound reduction on the lesioned side in cortical AChE activity and in the size of the releasable pool of [3H]ACh, neither the content nor the evoked release of glutamate was reduced significantly on the lesioned side. Furthermore, while oxotremorine strongly depressed the evoked release of [3H]ACh, it had no effect on the evoked release of endogenous glutamate measured simultaneously. These results do not support the co-transmitter role of glutamate in cortical cholinergic terminals, although they cannot statistically exclude that a small fraction of glutamate has a co-transmitter role, as proposed by Docherty et al.8. © 1990.