Differentiation of mitral cell dendrites in the developing main olfactory bulbs of normal and naris-occluded rats

Matsutani, Shinji; Yamamoto, Noboru

doi:10.1002/(sici)1096-9861(20000320)418:4<402::aid-cne3>3.0.co;2-g

Cited by 45 publications

(41 citation statements)

References 38 publications

(41 reference statements)

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“…Considering the prevailing hypothesis that defects in dendritic structural development lead to synaptic defects, we evaluated whether Mecp2 mutations alter the rate of maturation of MC dendrites, the primary target of OSN axons. In the OB, the maturation of MCs has been well characterized (Malun and Brunjes, 1996; Matsutani and Yamamoto, 2000; Blanchart et al, 2006). MC soma appears by E15, when the initial OSN axon segment is visible.…”

Section: Resultsmentioning

confidence: 99%

“…At P1, MCs extend many thin dendrites, and by P4 one of these dendrites has a thick shaft that visually stands out from the others. By P7, there is one remaining dendrite with an arborized tuft at its end and secondary processes extending into the external plexiform layer (EPL) (Malun and Brunjes, 1996; Matsutani and Yamamoto, 2000). …”

Section: Resultsmentioning

confidence: 99%

“…In newborn rodents, the majority of MC dendrites are ‘category A,’ displaying many thin processes. By P7-P10, the majority of MC dendrites are ‘category D,’ projecting a single dendrite with a tuft (Matsutani and Yamamoto, 2000; Imamura and Greer, 2009). We used this metric of maturation to assess whether disruptions in MeCP2 function directly affected the maturation of MCs.…”

Section: Resultsmentioning

confidence: 99%

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Normal mitral cell dendritic development in the setting of Mecp2 mutation

et al. 2012

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Rett Syndrome (RTT) is an autism spectrum disorder caused by mutation in the gene encoding methyl CpG binding protein 2 (MECP2). Evidence to date suggests that these disorders display defects in synaptic organization and plasticity. A hallmark of the pathology in RTT has been identified as decreased dendritic arborization, which has been interpreted to represent abnormal dendritic formation and pruning during development. Our previous studies revealed that olfactory axons display defective pathfinding and targeting in the setting of Mecp2 mutation. In the present work, we use Mecp2 mutant mouse models and the olfactory system to investigate dendritic development. Here, we demonstrate that mitral cell dendritic development proceeds normally in mutant mice, resulting in typical dendritic morphology at early postnatal ages. We also failed to detect abnormalities in dendritic inputs at symptomatic stages when glomeruli from mutant mice appear smaller in area than the WT (6 weeks postnatally). Collectively, these findings suggest that the initial defects in glomeruli impairment seen with Mecp2 mutation do not result from abnormal dendritic development. Our results using the olfactory system indicate that dendritic abnormalities are not an early feature in the abnormalities incurred by Mecp2 mutation.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Normal mitral cell dendritic development in the setting of Mecp2 mutation

et al. 2012

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“…16,23,27,34,51 Molecular signals guiding the formation of the LOT If the formation of the distinct olfactory structures and axons initially progresses independently, identifying developmental cues that control these processes might shed light on some of the more controversial points reviewed here. It is possible that axons from the AOB projection neurons, located deep within the LOT, could serve as pioneer axons to subsequently guide OB axons.…”

Section: Cell Death and Differentiationmentioning

confidence: 99%

The olfactory bulb as an independent developmental domain

López‐Mascaraque

Castro

2002

Cell Death Differ

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The olfactory system is a good model to study the mechanisms underlying guidance of growing axons to their appropriate targets. The formation of the olfactory bulb involves differentiation of several populations of cells and the initiation of the central projections, all under the temporal and spatial patterns of gene expression. Moreover, the nature of interactions between the olfactory epithelium, olfactory bulb and olfactory cortex at early developmental stages is currently of great interest. To explore these questions more fully, the present review aims to correlate recent data from different developmental studies, to gain insight into the mechanisms involved in the specification and development of the olfactory system. From our studies in the pax6 mutant mice (Sey Neu /Sey Neu ), it was concluded that the initial establishment of the olfactory bulb central projections is able to proceed independently of the olfactory sensory axons from the olfactory epithelium. The challenge that now remains is to consider the validity of the olfactory bulb as an independent development domain. In the course of evaluating these ideas, we will review the orchestra of molecular cues involved in the formation of the projection from the OB to the olfactory cortex.

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“…1C) (33). However, mitral cells from sensory-deprived animals had proportionately shorter apical dendrites and smaller glomerular diameters, consistent with impaired morphological development ( Fig.…”

Section: Sensory Experience and Electrical Coupling Between Mitral Cementioning

confidence: 99%

Experience-dependent maturation of the glomerular microcircuit

Maher

McGinley

Westbrook

2009

Proc. Natl. Acad. Sci. U.S.A.

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Spontaneous and patterned activity, largely attributed to chemical transmission, shape the development of virtually all neural circuits. However, electrical transmission also has an important role in coordinated activity in the brain. In the olfactory bulb, gap junctions between apical dendrites of mitral cells increase excitability and synchronize firing within each glomerulus. We report here that the development of the glomerular microcircuit requires both sensory experience and connexin (Cx)36-mediated gap junctions. Coupling coefficients, which measure electrical coupling between mitral cell dendrites, were high in young mice, but decreased after postnatal day (P)10 because of a maturational increase in membrane conductance. Sensory deprivation, induced by unilateral naris occlusion at birth, slowed the morphological development of mitral cells and arrested the maturational changes in membrane conductance and coupling coefficients. As the coupling coefficients decreased in normal mice, a glutamate-mediated excitatory postsynaptic current (EPSC) between mitral cells emerged by P30. Although mitral-mitral EPSCs were generally unidirectional, they were not present in young adult Cx36 ؊/؊ mice, suggesting that gap junctions are required for the development and/or function of the mature circuit. The experiencedependent transition from electrical transmission to combined chemical and electrical transmission provides a previously unappreciated mechanism that may tune the response properties of the glomerular microcircuit.connexin 36 ͉ gap junctions ͉ mitral cells ͉ olfactory ͉ EPSC

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Differentiation of mitral cell dendrites in the developing main olfactory bulbs of normal and naris-occluded rats

Cited by 45 publications

References 38 publications

Normal mitral cell dendritic development in the setting of Mecp2 mutation

Normal mitral cell dendritic development in the setting of Mecp2 mutation

The olfactory bulb as an independent developmental domain

Experience-dependent maturation of the glomerular microcircuit

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