Cargando…

Postnatal Development of Dendrodendritic Inhibition in the Mammalian Olfactory Bulb

The mitral–granule cell (MC–GC) reciprocal synapse is an important source of auto- and lateral-inhibition in the olfactory bulb (OB), and this local inhibition is critical for odor discrimination. We may gain insight into the role of MC autoinhibition in olfaction by correlating the functional devel...

Descripción completa

Detalles Bibliográficos
Autores principales: Dietz, Shelby B., Markopoulos, Foivos, Murthy, Venkatesh N.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Research Foundation 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3125518/
https://www.ncbi.nlm.nih.gov/pubmed/21738497
http://dx.doi.org/10.3389/fncel.2011.00010
_version_ 1782207230245863424
author Dietz, Shelby B.
Markopoulos, Foivos
Murthy, Venkatesh N.
author_facet Dietz, Shelby B.
Markopoulos, Foivos
Murthy, Venkatesh N.
author_sort Dietz, Shelby B.
collection PubMed
description The mitral–granule cell (MC–GC) reciprocal synapse is an important source of auto- and lateral-inhibition in the olfactory bulb (OB), and this local inhibition is critical for odor discrimination. We may gain insight into the role of MC autoinhibition in olfaction by correlating the functional development of the autoinhibition with the postnatal development of olfactory function. We have studied the functional development of the MC–GC reciprocal synapse using whole-cell patch-clamp recordings from MCs and GCs in acute OB slices from 3- to 30-day-old rats. The magnitude of dendrodendritic inhibition (DDI) measured by depolarizing a single MC and recording recurrent inhibition in the same cell increased up to the fifteenth day of life (P15), but dropped between P15 and P30. The initial increase and later decrease in DDI was echoed by a similar increase and decrease in the frequency of miniature inhibitory post-synaptic currents, suggesting an accompanying modulation in the number of synapses available to participate in DDI. The late decrease in DDI could also result, in part, from a decrease in GC excitability as well as an increase in relative contribution of N-methyl d-aspartate (NMDA) receptors to γ-amino butyric acid (GABA) release from GC synapses. Changes in release probability of GABAergic synapses are unlikely to account for the late reduction in DDI, although they might contribute to the early increase during development. Our results demonstrate that the functional MC–GC circuit evolves over development in a complex manner that may include both construction and elimination of synapses.
format Online
Article
Text
id pubmed-3125518
institution National Center for Biotechnology Information
language English
publishDate 2011
publisher Frontiers Research Foundation
record_format MEDLINE/PubMed
spelling pubmed-31255182011-07-07 Postnatal Development of Dendrodendritic Inhibition in the Mammalian Olfactory Bulb Dietz, Shelby B. Markopoulos, Foivos Murthy, Venkatesh N. Front Cell Neurosci Neuroscience The mitral–granule cell (MC–GC) reciprocal synapse is an important source of auto- and lateral-inhibition in the olfactory bulb (OB), and this local inhibition is critical for odor discrimination. We may gain insight into the role of MC autoinhibition in olfaction by correlating the functional development of the autoinhibition with the postnatal development of olfactory function. We have studied the functional development of the MC–GC reciprocal synapse using whole-cell patch-clamp recordings from MCs and GCs in acute OB slices from 3- to 30-day-old rats. The magnitude of dendrodendritic inhibition (DDI) measured by depolarizing a single MC and recording recurrent inhibition in the same cell increased up to the fifteenth day of life (P15), but dropped between P15 and P30. The initial increase and later decrease in DDI was echoed by a similar increase and decrease in the frequency of miniature inhibitory post-synaptic currents, suggesting an accompanying modulation in the number of synapses available to participate in DDI. The late decrease in DDI could also result, in part, from a decrease in GC excitability as well as an increase in relative contribution of N-methyl d-aspartate (NMDA) receptors to γ-amino butyric acid (GABA) release from GC synapses. Changes in release probability of GABAergic synapses are unlikely to account for the late reduction in DDI, although they might contribute to the early increase during development. Our results demonstrate that the functional MC–GC circuit evolves over development in a complex manner that may include both construction and elimination of synapses. Frontiers Research Foundation 2011-06-27 /pmc/articles/PMC3125518/ /pubmed/21738497 http://dx.doi.org/10.3389/fncel.2011.00010 Text en Copyright © 2011 Dietz, Markopoulos and Murthy. http://www.frontiersin.org/licenseagreement This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.
spellingShingle Neuroscience
Dietz, Shelby B.
Markopoulos, Foivos
Murthy, Venkatesh N.
Postnatal Development of Dendrodendritic Inhibition in the Mammalian Olfactory Bulb
title Postnatal Development of Dendrodendritic Inhibition in the Mammalian Olfactory Bulb
title_full Postnatal Development of Dendrodendritic Inhibition in the Mammalian Olfactory Bulb
title_fullStr Postnatal Development of Dendrodendritic Inhibition in the Mammalian Olfactory Bulb
title_full_unstemmed Postnatal Development of Dendrodendritic Inhibition in the Mammalian Olfactory Bulb
title_short Postnatal Development of Dendrodendritic Inhibition in the Mammalian Olfactory Bulb
title_sort postnatal development of dendrodendritic inhibition in the mammalian olfactory bulb
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3125518/
https://www.ncbi.nlm.nih.gov/pubmed/21738497
http://dx.doi.org/10.3389/fncel.2011.00010
work_keys_str_mv AT dietzshelbyb postnataldevelopmentofdendrodendriticinhibitioninthemammalianolfactorybulb
AT markopoulosfoivos postnataldevelopmentofdendrodendriticinhibitioninthemammalianolfactorybulb
AT murthyvenkateshn postnataldevelopmentofdendrodendriticinhibitioninthemammalianolfactorybulb