Document Detail


Regulation of glutamate release by heteromeric nicotinic receptors in layer V of the secondary motor region (Fr2) in the dorsomedial shoulder of prefrontal cortex in mouse.
MedLine Citation:
PMID:  23424068     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We studied how nicotinic acetylcholine receptors (nAChRs) regulate glutamate release in the secondary motor area (Fr2) of the dorsomedial murine prefrontal cortex, in the presence of steady agonist levels. Fr2 mediates response to behavioral situations that require immediate attention and is a candidate for generating seizures in the frontal epilepsies caused by mutant nAChRs. Morphological analysis showed a peculiar chemoarchitecture and laminar distribution of pyramidal cells and interneurons. Tonic application of 5 µM nicotine on Layer V pyramidal neurons strongly increased the frequency of spontaneous glutamatergic excitatory postsynaptic currents. The effect was inhibited by 1 µM dihydro-β-erythroidine (which blocks α4-containing nAChRs) but not by 10 nM methyllicaconitine (which blocks α7-containing receptors). Excitatory postsynaptic currents s were also stimulated by 5-iodo-3-[2(S)-azetidinylmethoxy]pyridine, selective for β2-containing receptors, in a dihydro-β-erythroidine -sensitive way. We next studied the association of α4 with different populations of glutamatergic terminals, by using as markers the vesicular glutamate transporter type (VGLUT) 1 for corticocortical synapses and VGLUT2 for thalamocortical projecting fibers. Immunoblots showed higher expression of α4 in Fr2, as compared with the somatosensory cortex. Immunofluorescence showed intense VGLUT1 staining throughout the cortical layers, whereas VGLUT2 immunoreactivity displayed a more distinct laminar distribution. In Layer V, colocalization of α4 nAChR subunit with both VGLUT1 and VGLUT2 was considerably stronger in Fr2 than in somatosensory cortex. Thus, in Fr2, α4β2 nAChRs are expressed in both intrinsic and extrinsic glutamatergic terminals and give a major contribution to control glutamate release in Layer V, in the presence of tonic agonist levels.
Authors:
Patrizia Aracri; Alida Amadeo; Maria Enrica Pasini; Umberto Fascio; Andrea Becchetti
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2013-03-19
Journal Detail:
Title:  Synapse (New York, N.Y.)     Volume:  67     ISSN:  1098-2396     ISO Abbreviation:  Synapse     Publication Date:  2013 Jun 
Date Detail:
Created Date:  2013-04-18     Completed Date:  2013-10-29     Revised Date:  2014-03-19    
Medline Journal Info:
Nlm Unique ID:  8806914     Medline TA:  Synapse     Country:  United States    
Other Details:
Languages:  eng     Pagination:  338-57     Citation Subset:  IM    
Copyright Information:
Copyright © 2013 Wiley Periodicals, Inc.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cerebral Cortex / cytology,  metabolism,  physiology*
Excitatory Postsynaptic Potentials / drug effects*
Gene Expression
Glutamic Acid / metabolism*
Interneurons / metabolism,  physiology
Mice
Nicotine / pharmacology
Nicotinic Agonists / pharmacology
Nicotinic Antagonists / pharmacology
Post-Synaptic Density / metabolism,  physiology
Pyramidal Cells / metabolism,  physiology
Receptors, Nicotinic / genetics,  metabolism*
Vesicular Glutamate Transport Protein 1 / genetics,  metabolism
Vesicular Glutamate Transport Protein 2 / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
GGP12147//Telethon
Chemical
Reg. No./Substance:
0/Nicotinic Agonists; 0/Nicotinic Antagonists; 0/Receptors, Nicotinic; 0/Slc17a6 protein, mouse; 0/Slc17a7 protein, mouse; 0/Vesicular Glutamate Transport Protein 1; 0/Vesicular Glutamate Transport Protein 2; 3KX376GY7L/Glutamic Acid; 54-11-5/Nicotine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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