Evidence map›Paper›PMID 34381336›Full record

ArticleFrontiers in cellular neuroscience2021

Alteration of Mesopontine Cholinergic Function by the Lack of KCNQ4 Subunit.

T Bayasgalan, S Stupniki, A Kovács, A Csemer, P Szentesi, K Pocsai, L Dionisio, G Spitzmaul, B Pál

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 55% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

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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

9 authors at 3 institutions in 2 countries.

T BayasgalanDepartment of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
S StupnikiInstituto de Investigaciones Bioquímicas de Bahía Blanca (INIBIBB), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad Nacional Del Sur (UNS), Bahía Blanca, Argentina.
A KovácsDepartment of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
A CsemerDepartment of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
P SzentesiDepartment of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
K PocsaiDepartment of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
L DionisioInstituto de Investigaciones Bioquímicas de Bahía Blanca (INIBIBB), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad Nacional Del Sur (UNS), Bahía Blanca, Argentina.
G SpitzmaulInstituto de Investigaciones Bioquímicas de Bahía Blanca (INIBIBB), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Universidad Nacional Del Sur (UNS), Bahía Blanca, Argentina.
B PálDepartment of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
University of Debrecen · HUConsejo Nacional de Investigaciones Científicas y Técnicas · ARUniversidad Nacional del Sur · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pedunculopontine nucleus (PPN), a structure known as a cholinergic member of the reticular activating system (RAS), is source and target of cholinergic neuromodulation and contributes to the regulation of the sleep-wakefulness cycle. The M-current is a voltage-gated potassium current modulated mainly by cholinergic signaling. KCNQ subunits ensemble into ion channels responsible for the M-current. In the central nervous system, KCNQ4 expression is restricted to certain brainstem structures such as the RAS nuclei. Here, we investigated the presence and functional significance of KCNQ4 in the PPN by behavioral studies and the gene and protein expressions and slice electrophysiology using a mouse model lacking KCNQ4 expression. We found that this mouse has alterations in the adaptation to changes in light-darkness cycles, representing the potential role of KCNQ4 in the regulation of the sleep-wakefulness cycle. As cholinergic neurons from the PPN participate in the regulation of this cycle, we investigated whether the cholinergic PPN might also possess functional KCNQ4 subunits. Although the M-current is an electrophysiological hallmark of cholinergic neurons, only a subpopulation of them had KCNQ4-dependent M-current. Interestingly, the absence of the KCNQ4 subunit altered the expression patterns of the other KCNQ subunits in the PPN. We also determined that, in wild-type animals, the cholinergic inputs of the PPN modulated the M-current, and these in turn can modulate the level of synchronization between neighboring PPN neurons. Taken together, the KCNQ4 subunit is present in a subpopulation of PPN cholinergic neurons, and it may contribute to the regulation of the sleep-wakefulness cycle.

Indexed as

KCNQ4 (Kv7.4)M-currentneuronal synchronizationnon-syndromic hearing loss (DFNA2)pedunculopontine nucleuspotassium channels

Identifiers

PMID34381336
PMCPMC8352570
OpenAlexW3183192607

What OpenQuestion holds

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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.