Evidence map›Paper›PMID 30320703›Full record

ArticleNeuroreport2018

Axon initial segment plasticity accompanies enhanced excitation of visual cortical neurons in aged rats.

Yanxia Ding, Ting Chen, Qin Wang, Yingying Yuan, Tianmiao Hua

Open access · hybridAbstract read
In one paragraph

Article in Neuroreport, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Brief Sensory Deprivation Triggers Cell Type-Specific Structural and Functional Plasticity in Olfactory Bulb Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  5. Article
  6. Article
  7. Trafficking mechanisms underlying NaChannels (Austin, Tex.) · 2020
    Review
  8. Article
  9. Article
  10. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Yanxia DingCollege of Life Sciences, Anhui Normal University.
Ting ChenCollege of Life Sciences, Anhui Normal University.
Qin WangCollege of Life Sciences, Anhui Normal University.
Yingying YuanCollege of Life Sciences, Anhui Normal University.
Tianmiao HuaCollege of Life Sciences, Anhui Normal University.
Anhui Normal University · CNGTx (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have indicated that the structure of the axon initial segment (AIS) of neurons is highly plastic in response to changes in neuronal activity. Whether an age-related enhancement of neuronal responses in the visual cortex is coupled with plasticity of AISs is unknown. Here, we compare the AIS length and the distribution of Nav1.6, a key Na ion channel in action potential (AP) initiation, along the AIS of layer II/III neurons in the primary visual cortex (V1) of young adult and aged rats, which were examined previously in a single-unit recording study. In that study, we found that V1 neurons in aged rats showed a significantly higher spontaneous activity and stronger visually evoked responses than did neurons in young rats. Our present study shows that the mean AIS length of layer II/III neurons in the V1 area of aged rats was significantly shorter than that of young adult rats. Further, the proportion of AIS with the Nav1.6 distribution was also reduced significantly in aged rats relative to young rats, as indicated by a decrease in the mean Nav1.6 immunofluorescence optical density within AISs and a specific decrease in Nav1.6 immunofluorescence optical density near the proximal region of the AIS. Our results indicate that aging results in both shortening of AISs and reduction of Nav1.6 Na ion channel distribution along AISs, which accompanies enhanced neuronal activity. This age-related morphological plasticity may lower the AP amplitude by reducing Na ion entry during AP initiation, spare ATPs consumed by Na ion pumps during membrane potential restoration, and thus balance the energy expenditure caused by an increased firing rate of cortical neurons during the aging process.

Indexed as

Action PotentialsAgingAnimalsAxon Initial SegmentMaleNAV1.6 Voltage-Gated Sodium ChannelNeuronal PlasticityNeuronsRatsRats, Sprague-DawleyVisual CortexNAV1.6 Voltage-Gated Sodium ChannelScn8a protein, rat

Identifiers

PMID30320703
PMCPMC6250279
OpenAlexW2897500417

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.