ArticleSchizophrenia bulletin2014
Chronic exposure of mutant DISC1 mice to lead produces sex-dependent abnormalities consistent with schizophrenia and related mental disorders: a gene-environment interaction study.
Article in Schizophrenia bulletin, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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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.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Chronic PbbioRxiv : the preprint server for biology · 2025Article
- Prenatal exposure to endocrine disrupting chemicals is associated with altered DNA methylation in cord blood.Epigenetics · 2022Article
- Chronic early-life lead exposure sensitizes adolescent rats to cocaine: Role of the dopaminergic system.Frontiers in molecular neuroscience · 2022Article
- Article
- Astrocyte Bioenergetics and Major Psychiatric Disorders.Advances in neurobiology · 2021Review
- Chronic developmental lead exposure increases μ-opiate receptor levels in the adolescent rat brain.Neurotoxicology · 2021Article
- (Ascorb)ing Pb Neurotoxicity in the Developing Brain.Antioxidants (Basel, Switzerland) · 2020Review
- Adolescent psychosocial stress enhances sensitization to cocaine exposure in genetically vulnerable mice.Neuroscience research · 2020Article
- Association of Typical Toxic Heavy Metals with Schizophrenia.International journal of environmental research and public health · 2019Article
- Preclinical neuroimaging of gene-environment interactions in psychiatric disease.The British journal of radiology · 2019Review
- Adolescent ΔBiological psychiatry · 2019Article
- Sensorimotor gating deficits in "two-hit" models of schizophrenia risk factors.Schizophrenia research · 2018Review
- DISC1 regulates lactate metabolism in astrocytes: implications for psychiatric disorders.Translational psychiatry · 2018Article
- Neurodevelopmental disease mechanisms, primary cilia, and endosomes converge on the BLOC-1 and BORC complexes.Developmental neurobiology · 2018Review
- Effects of genetic and environmental risk for schizophrenia on hippocampal activity and psychosis-like behavior in mice.Behavioural brain research · 2018Article
- A NewScientifica · 2018Article
- Effects of DISC1 Polymorphisms on Resting-State Spontaneous Neuronal Activity in the Early-Stage of Schizophrenia.Frontiers in psychiatry · 2018Article
- Adolescent stress leads to glutamatergic disturbance through dopaminergic abnormalities in the prefrontal cortex of genetically vulnerable mice.Psychopharmacology · 2017Article
- DISC1 in Astrocytes Influences Adult Neurogenesis and Hippocampus-Dependent Behaviors in Mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Article
- Utility and validity of DISC1 mouse models in biological psychiatry.Neuroscience · 2016Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The glutamatergic hypothesis of schizophrenia suggests that hypoactivity of the N-methyl-D-aspartate receptor (NMDAR) is an important factor in the pathophysiology of schizophrenia and related mental disorders. The environmental neurotoxicant, lead (Pb(2+)), is a potent and selective antagonist of the NMDAR. Recent human studies have suggested an association between prenatal Pb(2+) exposure and the increased likelihood of schizophrenia later in life, possibly via interacting with genetic risk factors. In order to test this hypothesis, we examined the neurobehavioral consequences of interaction between Pb(2+) exposure and mutant disrupted in schizophrenia 1 (mDISC1), a risk factor for major psychiatric disorders. Mutant DISC1 and control mice born by the same dams were raised and maintained on a regular diet or a diet containing moderate levels of Pb(2+). Chronic, lifelong exposure of mDISC1 mice to Pb(2+) was not associated with gross developmental abnormalities but produced sex-dependent hyperactivity, exaggerated responses to the NMDAR antagonist, MK-801, mildly impaired prepulse inhibition of the acoustic startle, and enlarged lateral ventricles. Together, these findings support the hypothesis that environmental toxins could contribute to the pathogenesis of mental disease in susceptible individuals.
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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 Socratic graph.