Research article summary (published 29 Jun 2001):

Inhibition of synaptically evoked cortical acetylcholine release by intracortical glutamate: involvement of GABAergic neurons.

Full Abstract

Cortical acetylcholine (ACh) has been shown to regulate diverse cognitive processes and its release can be regulated by neuromodulators that act presynaptically at cholinergic terminals. The neocortex receives dense glutamatergic input from thalamocortical and other fibres. The present study used in vivo microdialysis to examine, and pharmacologically characterize, the effect of glutamate on cortical ACh release evoked by electrical stimulation of the pedunculopontine tegmental nucleus in urethane-anaesthetized rats. All drugs were administered locally within the cortex by reverse dialysis. Application of glutamate had no detectable effect on spontaneous ACh release but reduced evoked cortical ACh efflux in a concentration-dependent manner. This effect was mimicked by the glutamate transporter blocker L-trans-pyrrolidine-2,4-dicarboxylic acid, as well as by the ionotropic glutamate receptor agonists N-methyl-D-aspartic acid and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid, and was blocked by the ionotropic glutamate receptor antagonists 6,7-dinitroquinoxaline-2,3-dione and (+/-)-3-(2-carboxypiperazin-4yl)-propyl-1-phosphonic acid. Glutamate application also increased extracellular adenosine levels but the simultaneous delivery of the broad-spectrum adenosine receptor antagonist caffeine failed to affect the inhibitory action of glutamate on evoked ACh release. However, the effect of glutamate was fully blocked by simultaneous delivery of the GABAA receptor antagonist bicuculline and partially blocked by the GABAB receptor antagonist phaclofen. These results suggest that ionotropic glutamate receptor activation by glutamate inhibits evoked cortical ACh release via an indirect pathway involving GABAergic neurons in the cortex.

Author information

Author/s: Materi, L M (LM); Semba, K (K);

Affiliation: Department of Anatomy and Neurobiology, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia B3H-4H7, Canada.

Journal and publication information

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

Journal: The European journal of neuroscience (Eur J Neurosci), published in France. (Language: eng)

Reference: 2001-Jul; vol 14 (issue 1) : pp 38-46

Dates: Created 2001/08/07; Completed 2001/09/27; Revised 2006/11/15;

PMID: 11488947, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Acetylcholine - metabolism; secretion Animals Basal Nucleus of Meynert - drug effects; metabolism; secretion Cerebral Cortex - cytology; drug effects; metabolism Cholinergic Fibers - drug effects; metabolism; secretion Electric Stimulation Excitatory Amino Acid Agonists - pharmacology Excitatory Amino Acid Antagonists - pharmacology GABA Agonists - pharmacology GABA Antagonists - pharmacology

Glutamic Acid - metabolism; pharmacology Male Neural Pathways - cytology; physiology Presynaptic Terminals - drug effects; metabolism; secretion Rats Rats, Wistar Receptors, GABA - drug effects; metabolism Receptors, Purinergic P1 - agonists; metabolism Tegmentum Mesencephali - cytology; physiology gamma-Aminobutyric Acid - metabolism

Associated Chemicals: Excitatory Amino Acid Agonists (0) ; Excitatory Amino Acid Antagonists (0) ; GABA Agonists (0) ; GABA Antagonists (0) ; Receptors, GABA (0) ; Receptors, Purinergic P1 (0) ; Acetylcholine (51-84-3) ; gamma-Aminobutyric Acid (56-12-2) ; Glutamic Acid (56-86-0)

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