ArticleOncotarget2016
Movement deficits and neuronal loss in basal ganglia in TRPC1 deficient mice.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
The trial behind it
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Whole-Brain Monosynaptic Inputs to and Axonal Projections From Posterior Insular Cortex GABAergic Neurons in Mice.CNS neuroscience & therapeutics · 2026Article
- Loss of endothelial TRPC1 aggravates metabolic dysfunction in obesity via disrupting adipose tissue homeostasis.Frontiers in molecular biosciences · 2025Article
- How TRPC Channels Modulate Hippocampal Function.International journal of molecular sciences · 2020Review
- RNA-seq analysis reveals TRPC genes to impact an unexpected number of metabolic and regulatory pathways.Scientific reports · 2020Article
- Transient Receptor Potential Channels as an Emerging Target for the Treatment of Parkinson's Disease: An Insight Into Role of Pharmacological Interventions.Frontiers in cell and developmental biology · 2020Review
- Quantitative whole-brain 3D imaging of tyrosine hydroxylase-labeled neuron architecture in the mouse MPTP model of Parkinson's disease.Disease models & mechanisms · 2019Article
- Inhibition of TRPC1-Dependent Store-Operated Calcium Entry Improves Synaptic Stability and Motor Performance in a Mouse Model of Huntington's Disease.Journal of Huntington's disease · 2018Article
- Activation of TRPC1 Channel by Metabotropic Glutamate Receptor mGluR5 Modulates Synaptic Plasticity and Spatial Working Memory.Frontiers in cellular neuroscience · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transient receptor potential cation (TRPC) channel proteins are abundantly expressed in brain. However, the functions of these TRPC proteins such as TRPC1 are largely unclear. In this study, we reported that TRPC1 deficiency caused movement disorder as measured by swimming test, modified open field test and sunflower seeds eating test. Immunofluorescent staining showed significant loss of both NeuN-positive cells and tyrosine hydroxylase (TH) -positive cells in the caudate putamen (CPu), the external globus pallidus (GPe), and the substantia nigra pars reticulata (SNr) in 5-month-old TRPC1 knockout mice (TRPC1-/-) compared to the wild type (WT) mice. TUNEL staining further revealed that TUNEL-positive cells were significantly increased in the CPu, GPe, and SNr of TRPC1-/- mice. Taken together, these data suggests that TRPC1 is involved in the control of motor function by inhibiting the apoptosis of neuronal cells of basal ganglia.
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Registered trials
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.