Document Detail


Loss of olfactory cell adhesion molecule reduces the synchrony of mitral cell activity in olfactory glomeruli.
MedLine Citation:
PMID:  21486802     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Odours generate activity in olfactory receptor neurons, whose axons contact the dendritic tufts of mitral cells within olfactory bulb glomeruli. These axodendritic synapses are anatomically separated from dendrodendritic synapses within each glomerulus. Mitral cells within a glomerulus show highly synchronized activity as assessed with whole-cell recording from pairs of mitral cells. We examined glomerular activity in mice lacking the olfactory cell adhesion molecule (OCAM). Glomeruli in mice lacking OCAM show a redistribution of synaptic subcompartments, but the total area occupied by axonal inputs was similar to wild-type mice. Stimulation of olfactory nerve bundles showed that excitatory synaptic input to mitral cells as well as dendrodendritic inhibition was unaffected in the knockout. However, correlated spiking in mitral cells was significantly reduced, as was electrical coupling between apical dendrites. To analyse slow network dynamics we induced slow oscillations with a glutamate uptake blocker. Evoked and spontaneous slow oscillations in mitral cells and external tufted cells were broader and had multiple peaks in OCAM knockout mice, indicating that synchrony of slow glomerular activity was also reduced. To assess the degree of shared activity between mitral cells under physiological conditions, we analysed spontaneous sub-threshold voltage oscillations using coherence analysis. Coherent activity was markedly reduced in cells from OCAM knockout mice across a broad range of frequencies consistent with a decrease in tightly time-locked activity. We suggest that synchronous activity within each glomerulus is dependent on segregation of synaptic subcompartments.
Authors:
Maria Borisovska; Matthew J McGinley; AeSoon Bensen; Gary L Westbrook
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-02-21
Journal Detail:
Title:  The Journal of physiology     Volume:  589     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-04-18     Completed Date:  2011-08-09     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1927-41     Citation Subset:  IM    
Affiliation:
Vollum Institute, Oregon Health and Science University, Portland, OR 97239, USA. maria.borisovska@gmail.com
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Electric Stimulation
Excitatory Postsynaptic Potentials
Glutamic Acid / metabolism
Inhibitory Postsynaptic Potentials
Kinetics
Luminescent Proteins / biosynthesis,  genetics
Mice
Mice, 129 Strain
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Neural Cell Adhesion Molecules / deficiency*,  genetics
Neural Inhibition
Neural Pathways / metabolism
Neurotransmitter Agents / pharmacology
Olfactory Bulb / drug effects,  metabolism*
Patch-Clamp Techniques
Periodicity
Reaction Time
Smell*
Synaptic Transmission* / drug effects
gamma-Aminobutyric Acid / metabolism
Grant Support
ID/Acronym/Agency:
NS02694/NS/NINDS NIH HHS; P30 NS061800/NS/NINDS NIH HHS; R01 NS026494/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Luminescent Proteins; 0/Ncam2 protein, mouse; 0/Neural Cell Adhesion Molecules; 0/Neurotransmitter Agents; 56-12-2/gamma-Aminobutyric Acid; 56-86-0/Glutamic Acid
Comments/Corrections

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