Evidence map›Paper›PMID 22745484›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Tbr2 deficiency in mitral and tufted cells disrupts excitatory-inhibitory balance of neural circuitry in the mouse olfactory bulb.

Rumiko Mizuguchi, Hiromi Naritsuka, Kensaku Mori, Chai-An Mao, William H Klein, Yoshihiro Yoshihara

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 47 citations in OpenAlex.

  1. TheiScience · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Effects of nasal inflammation on the olfactory bulb.Journal of neuroinflammation · 2022
    Review
  6. Article
  7. Article
  8. Characterization of Tbr2-expressing retinal ganglion cells.The Journal of comparative neurology · 2021
    Article
  9. Generation and Characterization of a Cell Type-Specific, Inducible Cre-Driver Line to Study Olfactory Processing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. RNA-seq analysis of developing olfactory bulb projection neurons.Molecular and cellular neurosciences · 2016
    Article
4 · The record

Corrections and comments

  • Erratum issued
    Mao, Chai-An [added]; Klein, William H [added]
5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Rumiko MizuguchiLaboratory for Neurobiology of Synapse, RIKEN Brain Science Institute, Saitama 351-0198, Japan.
Hiromi Naritsuka
Kensaku Mori
Chai-An Mao
William H Klein
Yoshihiro Yoshihara
RIKEN Center for Brain Science · JPThe University of Tokyo · JP

Funding

Optic nerve regeneration: gene networks in retina developmentR01EY011930 · NEI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI KLEIN, WILLIAM H. · 1997 to 2016
$5.3M
NEI NIH HHS EY011930NEI NIH HHS R01 EY011930
6 · The paper itself

Abstract

The olfactory bulb (OB) is the first relay station in the brain where odor information from the olfactory epithelium is integrated, processed through its intrinsic neural circuitry, and conveyed to higher olfactory centers. Compared with profound mechanistic insights into olfactory axon wiring from the nose to the OB, little is known about the molecular mechanisms underlying the formation of functional neural circuitry among various types of neurons inside the OB. T-box transcription factor Tbr2 is expressed in various types of glutamatergic excitatory neurons in the brain including the OB projection neurons, mitral and tufted cells. Here we generated conditional knockout mice in which the Tbr2 gene is inactivated specifically in mitral and tufted cells from late embryonic stages. Tbr2 deficiency caused cell-autonomous changes in molecular expression including a compensatory increase of another T-box member, Tbr1, and a concomitant shift of vesicular glutamate transporter (VGluT) subtypes from VGluT1 to VGluT2. Tbr2-deficient mitral and tufted cells also exhibited anatomical abnormalities in their dendritic morphology and projection patterns. Additionally, several non-cell-autonomous phenotypes were observed in parvalbumin-, calbindin-, and 5T4-positive GABAergic interneurons. Furthermore, the number of dendrodendritic reciprocal synapses between mitral/tufted cells and GABAergic interneurons was significantly reduced. Upon stimulation with odorants, larger numbers of mitral and tufted cells were activated in Tbr2 conditional knockout mice. These results suggest that Tbr2 is required for not only the proper differentiation of mitral and tufted cells, but also for the establishment of functional neuronal circuitry in the OB and maintenance of excitatory-inhibitory balance crucial for odor information processing.

Indexed as

AnimalsCadherinsDendritesFluorescent DyesGene Expression RegulationGreen Fluorescent ProteinsInterneuronsMaleMiceMice, TransgenicNeural InhibitionNeuronsNF-kappa BOdorantsOlfactory BulbReceptors, OdorantCadherinsenhanced green fluorescent proteinEomes protein, mouseFluorescent DyesGreen Fluorescent ProteinsNF-kappa BReceptors, OdorantT-Box Domain ProteinsTranscription FactorsVesicular Glutamate Transport Proteins

Identifiers

PMID22745484
PMCPMC3700647
OpenAlexW2051369017

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.