Is glutamate a co-transmitter 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 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.
Szerb
J C
JC
Department of Physiology and Biophysics, Dalhousie University, Halifax, N.S., Canada.
Fine
A
A
D000109:Acetylcholine / Q000493:pharmacokinetics; D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D001479:Basal Ganglia / Q000502:physiology*; D002540:Cerebral Cortex / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D002799:Cholinergic Fibers / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D005971:Glutamates / Q000378:metabolism* / Q000502:physiology; D018698:Glutamic Acid; D018377:Neurotransmitter Agents / Q000378:metabolism* / Q000502:physiology; D010095:Oxotremorine / Q000494:pharmacology*; D051381:Rats
D005971:Glutamates; D018377:Neurotransmitter Agents; D018698:Glutamic Acid; D010095:Oxotremorine; D000110:Acetylcholinesterase; D000109:Acetylcholine