Evidence map›Paper›PMID 28948610›Full record

ArticleThe Journal of physiology2017

The α

Minoru Ohshima, Chiaki Itami, Fumitaka Kimura

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Alpha-adrenergic receptor activation after fetal hypoxia-ischaemia suppresses transient epileptiform activity and limits loss of oligodendrocytes and hippocampal neurons.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Article
  7. Review
  8. Article
  9. Axo-axonic synapses: Diversity in neural circuit function.The Journal of comparative neurology · 2021
    Review
  10. Review
  11. 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

3 authors at 3 institutions in 1 country.

Minoru OhshimaDepartment of Physiology, Kansai University of Health Sciences, Kumatori, 590-0482, Japan.
Chiaki ItamiDepartment of Physiology, Faculty of Medicine, Saitama Medical University, Moroyama, Saitama, 350-0495, Japan.
Fumitaka KimuraDepartment of Molecular Neuroscience, Osaka University Graduate School of Medicine, Suita, 565-0871, Japan.ORCID 0000-0002-7420-428X
Kansai University of Nursing and Health Sciences · JPSaitama Medical University · JPThe University of Osaka · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

key pointsThe effects of noradrenaline on excitatory synaptic transmission to regular spiking (excitatory) cells as well as regular spiking non-pyramidal and fast spiking (both inhibitory) cells in cortical layer 4 were studied in thalamocortical slice preparations, focusing on vertical input from thalamus and layer 2/3 in the mouse barrel cortex. Excitatory synaptic responses were suppressed by noradrenaline. However, currents induced by iontophoretically applied glutamate were not suppressed. Further, paired pulse ratio and coefficient of variation analysis indicated the site of action was presynaptic. Pharmacological studies indicated that the suppression was mediated by the α ABSTRACT: The mammalian neocortex is widely innervated by noradrenergic (NA) fibres from the locus coeruleus. To determine the effects of NA on vertical synaptic inputs to layer 4 (L4) cells from the ventrobasal thalamus and layer 2/3 (L2/3), thalamocortical slices were prepared and whole-cell recordings were made from L4 cells. Excitatory synaptic responses were evoked by electrical stimulation of the thalamus or L2/3 immediately above. Recorded cells were identified as regular spiking, regular spiking non-pyramidal or fast spiking cells through their firing patterns in response to current injections. NA suppressed (∼50% of control) excitatory vertical inputs to all cell types in a dose-dependent manner. The presynaptic site of action of NA was suggested by three independent studies. First, responses caused by iontophoretically applied glutamate were not suppressed by NA. Second, the paired pulse ratio was increased during NA suppression. Finally, a coefficient of variation (CV) analysis was performed and the resultant diagonal alignment of the ratio of CV

Indexed as

Excitatory Postsynaptic PotentialsAdrenergic alpha-2 Receptor AgonistsAdrenergic alpha-2 Receptor AntagonistsAdrenergic beta-AntagonistsAdrenergic FibersAnimalsGlutamic AcidMiceMice, Inbred C57BLNeocortexNeuronsNorepinephrinePhenylephrinePrazosinPropranololReceptors, Adrenergic, alpha-2Adrenergic alpha-2 Receptor AgonistsAdrenergic alpha-2 Receptor AntagonistsAdrenergic beta-AntagonistsGlutamic AcidNorepinephrinePhenylephrinePrazosinPropranololReceptors, Adrenergic, alpha-2Yohimbinealpha 2A-KOEPSCmousenoradrenalinepresynaptic inhibitionthalamocortical

Identifiers

PMID28948610
PMCPMC5685826
OpenAlexW2760111553

What OpenQuestion holds

Textmetadata
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.