Is glutamate a co-transmitter in cortical cholinergic terminals? Effects of nucleus basalis lesion and of presynaptic muscarinic agents.

Article date: 1990/5/7

PubMed ID: 1972643

Journal name: Brain research (ISSN: 0006-8993)


To obtain additional evidence in support of the co-transmitter role of glutamate in cortical cholinergic terminals proposed by Docherty et al., the right nucleus basalis in rats was lesioned with ibotenic acid; resulting changes in cortical acetylcholinesterase (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.

Author List: Szerb J C, Fine A

Publication Types: Journal Article; Research Support, Non-U.S. Gov't

Substances mentioned in the article: Glutamates; Neurotransmitter Agents; Glutamic Acid; Oxotremorine; Acetylcholinesterase; Acetylcholine;

Mesh terms: Acetylcholine/pharmacokinetics; Acetylcholinesterase/metabolism; Animals; Basal Ganglia/physiology; Cerebral Cortex/cytology; Cholinergic Fibers/drug effects; Glutamates/metabolism; Glutamic Acid; Neurotransmitter Agents/metabolism; Oxotremorine/pharmacology; Rats;

1972643.txt · Last modified: 2018/11/20 14:26 (external edit)