Evidence map›Paper›PMID 37852390›Full record

ArticleNeurobiology of disease2023

Feed-forward metabotropic signaling by Cav1 Ca

C Tubert, E Zampese, T Pancani, T Tkatch, D J Surmeier

Open access · goldAbstract read
In one paragraph

Article in Neurobiology of disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Levodopa treatment: impacts and mechanisms throughout Parkinson's disease progression.Journal of neural transmission (Vienna, Austria : 1996) · 2025
    Review
  4. Article
  5. Article
  6. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

C TubertDepartment of Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Universidad de Buenos Aires - CONICET. Instituto de Fisiología y Biofísica Bernardo Houssay (IFIBIO Houssay), Facultad de Medicina, Departamento de Ciencias Fisiológicas, Grupo de Neurociencia de Sistemas, Buenos Aires, Argentina.
E ZampeseDepartment of Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
T PancaniDepartment of Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Max Planck Florida Institute for Neuroscience, 1 Max Planck Way, Jupiter, FL 33458, USA.
T TkatchDepartment of Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
D J SurmeierDepartment of Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD 20815, USA. Electronic address: j-surmeier@northwestern.edu.
Northwestern University · USResearch Network (United States) · USUniversity of Buenos Aires · AR

Funding

General Motor Control Mechanisms and Disease Training ProgramT32NS041234 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BEVAN, MARK D · 2001 to 2022
$6.0M
Determinants of Basal Ganglia Pathology in Parkinson's DiseaseR01NS121174 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BEVAN, MARK D, SURMEIER, DALTON JAMES · 2021 to 2025
$3.6M
NINDS NIH HHS R01 NS121174NINDS NIH HHS T32 NS041234
6 · The paper itself

Abstract

Like a handful of other neuronal types in the brain, cholinergic neurons (CNs) in the pedunculopontine nucleus (PPN) are lost during Parkinson's disease (PD). Why this is the case is unknown. One neuronal trait implicated in PD selective neuronal vulnerability is the engagement of feed-forward stimulation of mitochondrial oxidative phosphorylation (OXPHOS) to meet high bioenergetic demand, leading to sustained oxidant stress and ultimately degeneration. The extent to which this trait is shared by PPN CNs is unresolved. To address this question, a combination of molecular and physiological approaches were used. These studies revealed that PPN CNs are autonomous pacemakers with modest spike-associated cytosolic Ca

Indexed as

Parkinson DiseaseAdenosine TriphosphateCholinergic NeuronsHumansOxidantsSignal TransductionAdenosine TriphosphateOxidantsATP-sensitive K(+) channelsCalcium voltage-dependent channelsMitocondrial oxidative phosphorilationParkinson's diseasePPN cholinergic neurons

Identifiers

PMID37852390
PMCPMC10792542
OpenAlexW4387675855

What OpenQuestion holds

Textmetadata
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.