Evidence map›Paper›PMID 27178196›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2016

Corticothalamic Spike Transfer via the L5B-POm Pathway in vivo.

Rebecca A Mease, Anton Sumser, Bert Sakmann, Alexander Groh

Abstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Article
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  10. Dissection of brain-wide resting-state and functional somatosensory circuits by fMRI with optogenetic silencing.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  11. Review
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  16. Sense and Action across the Layers of the Rat Posterior Parietal Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  17. Review
  18. Article
  19. Trans-thalamic Pathways: Strong Candidates for Supporting Communication between Functionally Distinct Cortical Areas.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
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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

4 authors.

Rebecca A MeaseInstitute for Neuroscience of the Technische Universität München, 80802 Munich, Germany Department of Neurosurgery, Klinikum rechts der Isar, Technische Universität München, 81675 Munich, Germany.
Anton SumserInstitute for Neuroscience of the Technische Universität München, 80802 Munich, Germany.
Bert SakmannInstitute for Neuroscience of the Technische Universität München, 80802 Munich, Germany Max Planck Institute for Neurobiology, 82152 Martinsried, Germany.
Alexander GrohInstitute for Neuroscience of the Technische Universität München, 80802 Munich, Germany Department of Neurosurgery, Klinikum rechts der Isar, Technische Universität München, 81675 Munich, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cortex connects to the thalamus via extensive corticothalamic (CT) pathways, but their function in vivo is not well understood. We investigated "top-down" signaling from cortex to thalamus via the cortical layer 5B (L5B) to posterior medial nucleus (POm) pathway in the whisker system of the anesthetized mouse. While L5B CT inputs to POm are extremely strong in vitro, ongoing activity of L5 neurons in vivo might tonically depress these inputs and thereby block CT spike transfer. We find robust transfer of spikes from the cortex to the thalamus, mediated by few L5B-POm synapses. However, the gain of this pathway is not constant but instead is controlled by global cortical Up and Down states. We characterized in vivo CT spike transfer by analyzing unitary PSPs and found that a minority of PSPs drove POm spikes when CT gain peaked at the beginning of Up states. CT gain declined sharply during Up states due to frequency-dependent adaptation, resulting in periodic high gain-low gain oscillations. We estimate that POm neurons receive few (2-3) active L5B inputs. Thus, the L5B-POm pathway strongly amplifies the output of a few L5B neurons and locks thalamic POm sub-and suprathreshold activity to cortical L5B spiking.

Indexed as

Action PotentialsAnesthesiaAnimalsComputer SimulationExcitatory Postsynaptic PotentialsGABA-A Receptor AgonistsMice, TransgenicMicroelectrodesModels, NeurologicalMuscimolNeural PathwaysNeuroanatomical Tract-Tracing TechniquesNeuronsOptogeneticsSomatosensory CortexThalamusGABA-A Receptor AgonistsMuscimolVesicular Inhibitory Amino Acid Transport ProteinsViaat protein, mouseadaptationbarrel cortexcorticothalamic feedbacklayer 5POmsomatosensory systemthy-1VGAT

Identifiers

PMID27178196
PMCPMC4961018

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Registered trials

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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.