Cited by 4Neuroscience and Neuropharmacology ResearchNeurogenesis and neuroplasticity mechanismsOlfactory and Sensory Function Studies

Activity-dependent synaptic competition and dendrite pruning in developing mitral cells

Open access
Imai, Takeshi·2025·Frontiers in Neural Circuits

Abstract

During the early postnatal period, neurons in sensory circuits dynamically remodel their connectivity to acquire discrete receptive fields. Neuronal activity is thought to play a central role in circuit remodeling during this period: Neuronal activity stabilizes some synaptic connections while eliminating others. Synaptic competition plays a central role in the binary choice between stabilization and elimination. While activity-dependent “punishment signals” propagating from winner to loser synapses have been hypothesized to drive synapse elimination, their exact nature has remained elusive. In this review, I summarize recent studies in mouse mitral cells that explain how only one dendrite is stabilized while others are eliminated, based on early postnatal spontaneous activity in the olfactory bulb. I discuss how the hypothetical punishment signals act on loser but not winner dendrites to establish only one primary dendrite per mitral cell, the anatomical basis for the odorant receptor-specific parallel information processing in the olfactory bulb.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3389/fncir.2025.1541926

Cites

83 of 83 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Other eat me signals include phosphatidylserine exposure on dendrites, recognized by microglial TREM2, and CX3CR1/CX3CL1 signaling, which helps identify synapses for elimination.

    “Other “eat me” signals include phosphatidylserine (PS) exposure on dendrites, recognized by microglial TREM2, and CX3CR1/CX3CL1 signaling, which helps identify synapses for elimination [81,82,83].”

    From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [83]

    The “Role of glia in synapse elimination” section discusses proposed “eat-me” signals on loser synapses and reports that microglia can engulf synapses. It does not identify phosphatidylserine, TREM2, or CX3CR1/CX3CL1 as those signals or explain their proposed roles. The section also cautions that microglia are dispensable for dendrite pruning in the circuits discussed. (LLM, conf=0.82)

    Experimental — accuracy not yet measured
  • Tagged synapses are recognized and engulfed by microglial complement receptor 3 (CR3).

    “These tagged synapses are then recognized and engulfed by microglial complement receptor 3 (CR3).”

    From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [83]

    The ‘Role of glia in synapse elimination’ section reports that microglia engulf synapses in some circuits and discusses a proposed role for ‘eat-me’ signals on loser synapses. It does not identify complement receptor 3 (CR3) as the receptor that recognizes tagged synapses, and it cautions that microglial involvement in synapse elimination may have been overstated. No page number was supplied for the passage. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • Complement proteins, particularly C1q and C3, are produced by microglia or astrocytes and localize to apoptotic, immature, or weak developing synapses.

    “Complement proteins, particularly C1q (the initiating protein) and C3, are produced by microglia or astrocytes and localize to apoptotic, immature, or weak developing synapses.”

    From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [83]

    The ‘Role of glia in synapse elimination’ section discusses glial engulfment of synapses, but does not say that microglia or astrocytes produce C1q or C3, or that those proteins localize to apoptotic, immature, or weak synapses. Searches for C1q, C3, and complement localization found only complement-related reference titles, not a passage addressing the claim. (LLM, conf=0.76)

    Experimental — accuracy not yet measured
  • C1q presynaptic tagging correlates with apoptotic markers, guiding pruning decisions.

    “C1q presynaptic tagging correlates with apoptotic markers, guiding pruning decisions [81,82,83].”

    From Molecular Physiology of the Neuronal Synapse (2026) · cites this paper as [83]

    The ‘Role of glia in synapse elimination’ section discusses proposed eat-me signals and microglial engulfment, but does not describe C1q tagging or a correlation with apoptotic markers. Searches for C1q, complement tagging, and apoptotic markers found no passage establishing the claimed relationship. (LLM, conf=0.73)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Imai, T.
Affiliations
Kyushu University (JP)
Corresponding author
Imai, Takeshi
Venue
Frontiers in Neural Circuits
Published
2025-01-27
Volume
19
Pages
1541926-1541926
ISSN
1662-5110 (ISSN-L)
OpenAlex
W4406850269
Cited by
4
References
83
Citations by year
2026: 3 · 2025: 1
FWCI
0.48
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Neural Circuits (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Ministry of Education, Culture, Sports, Science and Technology
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Neuroscience › Sensory Systems › Olfactory and Sensory Function Studies
Keywords
synaptic competition, dendrite pruning, mitral cells, olfactory bulb, postnatal development, spontaneous activity, synaptic pruning, primary dendrites, parallel information processing
MeSH terms
Animals, Dendrites, Neuronal Plasticity, Olfactory Bulb, Synapses, Mice, Neurogenesis

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review