Increased hippocampal acetylcholine release during a working memory task

doi:10.1016/0014-2999(96)00289-0

European Journal of Pharmacology

Volume 307, Issue 2, 27 June 1996, Pages R1-R2

https://doi.org/10.1016/0014-2999(96)00289-0 Get rights and content

Abstract

In this study we examined whether the food-reinforced alternation performance was associated with increased acetylcholine output in the dorsal hippocampus. Rats were trained to acquire the task using a T-maze. The control group consisted of rats introduced into the T-maze to run only on the day of dialysis. Acetylcholine release increased significantly in control rats only in the first 10 min after they were put into the T-maze. In trained rats acetylcholine output increased in the waiting cage as well as during trials in the T-maze. The increase in acetylcholine output in rats that had learned the task was significantly greater than in control rats.

References (8)

J. Day et al.
Cholinergic activity in the rat hippocampus, cortex and striatum correlates with locomotor activity: an in vivo microdialysis study
Pharmacol. Biochem. Behav.
(1991)
S.B. Dunnett et al.
Septal transplants restore maze learning in rats with fornixfimbria lesions
Brain Res.
(1982)
A. Imperato et al.
Effect of cocaine and amphetamine on acetylcholine release in the hippocampus and caudate nucleus
Eur. J. Pharmacol.
(1993)
G. Damsma et al.
A simple and economic assay for choline and acetylcholine using HPLC, an enzyme reactor and an electrochemical detector
J. Neurochem.
(1985)

There are more references available in the full text version of this article.

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Rapid communicationIncreased hippocampal acetylcholine release during a working memory task

Abstract

Pharmacol. Biochem. Behav.

Brain Res.

Eur. J. Pharmacol.

A simple and economic assay for choline and acetylcholine using HPLC, an enzyme reactor and an electrochemical detector

J. Neurochem.

Rapid communication
Increased hippocampal acetylcholine release during a working memory task