Linked Life Data

11488947

Source:http://linkedlifedata.com/resource/pubmed/id/11488947

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-8-7
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0953-816X
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
38-46
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:11488947-Acetylcholine, pubmed-meshheading:11488947-Animals, pubmed-meshheading:11488947-Basal Nucleus of Meynert, pubmed-meshheading:11488947-Cerebral Cortex, pubmed-meshheading:11488947-Cholinergic Fibers, pubmed-meshheading:11488947-Electric Stimulation, pubmed-meshheading:11488947-Excitatory Amino Acid Agonists, pubmed-meshheading:11488947-Excitatory Amino Acid Antagonists, pubmed-meshheading:11488947-GABA Agonists, pubmed-meshheading:11488947-GABA Antagonists, pubmed-meshheading:11488947-Glutamic Acid, pubmed-meshheading:11488947-Male, pubmed-meshheading:11488947-Neural Pathways, pubmed-meshheading:11488947-Presynaptic Terminals, pubmed-meshheading:11488947-Purinergic P1 Receptor Agonists, pubmed-meshheading:11488947-Rats, pubmed-meshheading:11488947-Rats, Wistar, pubmed-meshheading:11488947-Receptors, GABA, pubmed-meshheading:11488947-Receptors, Purinergic P1, pubmed-meshheading:11488947-Tegmentum Mesencephali, pubmed-meshheading:11488947-gamma-Aminobutyric Acid
pubmed:year
2001
pubmed:articleTitle
Inhibition of synaptically evoked cortical acetylcholine release by intracortical glutamate: involvement of GABAergic neurons.
pubmed:affiliation
Department of Anatomy and Neurobiology, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia B3H-4H7, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't