ReviewProgress in neurobiology2012
CACNA1C (Cav1.2) in the pathophysiology of psychiatric disease.
Review in Progress in neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers, 5 of them syntheses that pooled 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.
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.
Who cites it
157 citing papers in PubMed, 5 syntheses or guidelines pooled it, 272 citations in OpenAlex.
- Autism spectrum disorder and schizophrenia: An updated conceptual review.Autism research : official journal of the International Society for Autism Research · 2022Pooled it
- Genome-wide association analysis of self-reported daytime sleepiness identifies 42 loci that suggest biological subtypes.Nature communications · 2019Pooled it
- CACNA1C (rs1006737) may be a susceptibility gene for schizophrenia: An updated meta-analysis.Brain and behavior · 2019Pooled it
- Meta-Analysis of Public Microarray Datasets Reveals Voltage-Gated Calcium Gene Signatures in Clinical Cancer Patients.PloS one · 2015Pooled it
- Association of a miRNA-137 polymorphism with schizophrenia in a Southern Chinese Han population.BioMed research international · 2014Pooled it
- CACNA1C polymorphisms Impact Cognitive Recovery in Patients with Bipolar Disorder in a Six-week Open-label Trial.Scientific reports · 2017Trial
- Ionic Homeostasis Failure in Major Depressive Disorder: Ion Channel Mechanisms, Excitation-Inhibition Imbalance, and Precision Therapeutics.International journal of molecular sciences · 2026Review
- Article
- Cacna1c deficiency in parvalbumin-expressing neurons promotes anxiety and passive stress-coping behavior.Scientific reports · 2026Article
- Cross-Species evidence for hippocampal CACNA1C as a therapeutic target for alcohol use disorder.Translational psychiatry · 2026Article
- Article
- Bipolar disorder in an evolutionary framework: rethinking adaptation, vulnerability, and stigma.Frontiers in psychiatry · 2026Article
- Dysregulation of neurodevelopmental regulatory networks in Anorexia Nervosa: an integrated multi-layered omics analysis.Frontiers in cell and developmental biology · 2026Article
- Molecular Signatures of Early-Onset Bipolar Disorder and Schizophrenia: Transcriptomic and Machine-Learning Insights into Calcium and cAMP Signaling, Including Sex-Specific Patterns.International journal of molecular sciences · 2025Article
- Stimulation of CaScience signaling · 2025Article
- Astrocytic abnormalities in brain-specificChannels (Austin, Tex.) · 2025Article
- A Macrophage-Derived Factor on Human iPSC-Derived Cardiomyocyte Function: The Role of Osteopontin.Cells · 2025Article
- A review of post-GWAS studies in schizophrenia.Translational psychiatry · 2025Review
- The Impact of Overexpression of the Mouse Ortholog ofBiological psychiatry global open science · 2025Article
- Pathophysiologic Mechanisms of Cardiovascular Disease in Patients With Bipolar Disorder.Cureus · 2025Review
97 more citing papers are in PubMed but not listed here.
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 2 institutions in 1 country.
Funding
Abstract
One of the most consistent genetic findings to have emerged from bipolar disorder genome wide association studies (GWAS) is with CACNA1C, a gene that codes for the α(1C) subunit of the Ca(v)1.2 voltage-dependent L-type calcium channel (LTCC). Genetic variation in CACNA1C have also been associated with depression, schizophrenia, autism spectrum disorders, as well as changes in brain function and structure in control subjects who have no diagnosable psychiatric illness. These data are consistent with a continuum of shared neurobiological vulnerability between diverse-Diagnostic and Statistical Manual (DSM) defined-neuropsychiatric diseases. While involved in numerous cellular functions, Ca(v)1.2 is most frequently implicated in coupling of cell membrane depolarization to transient increase of the membrane permeability for calcium, leading to activation and, potentially, changes in intracellular signaling pathway activity, gene transcription, and synaptic plasticity. Ca(v)1.2 is involved in the proper function of numerous neurological circuits including those involving the hippocampus, amygdala, and mesolimbic reward system, which are strongly implicated in psychiatric disease pathophysiology. A number of behavioral effects of LTCC inhibitors have been described including antidepressant-like behavioral actions in rodent models. Clinical studies suggest possible treatment effects in a subset of patients with mood disorders. We review the genetic structure and variation of CACNA1C, discussing relevant human genetic and clinical findings, as well as the biological actions of Ca(v)1.2 that are most relevant to psychiatric illness.
Indexed as
Identifiers
What OpenQuestion holds
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.