ArticleFrontiers in psychiatry2019
Disrupted-in-Schizophrenia 1 (DISC1) Overexpression and Juvenile Immune Activation Cause Sex-Specific Schizophrenia-Related Psychopathology in Rats.
Article in Frontiers in psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Epigenetic Evidence Implies Disturbed Proteostasis and Potentially Protein Aggregation in Suicidality.Biomolecules · 2026Review
- Pharmacological rescue of social deficits in rats featuring Disrupted-in-Schizophrenia-1 (DISC1) protein aggregation.Schizophrenia (Heidelberg, Germany) · 2026Article
- Social Reward Learning Deficits and Concordant Brain Alterations in Rats Overexpressing Disrupted-in-Schizophrenia 1 (DISC1).The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Peering into the mind: unraveling schizophrenia's secrets using models.Molecular psychiatry · 2025Review
- Decoding the Molecular Mechanisms of miRNAs: Protein Interactions in Schizophrenia Pathogenesis.Current protein & peptide science · 2025Review
- Monozygotic twins discordant for schizophrenia differ in maturation and synaptic transmission.Molecular psychiatry · 2024Article
- 50-kHz ultrasonic vocalizations do not signal social anhedonia in transgenic DISC1 rats.Brain and behavior · 2023Article
- Sex Differences in Psychosis: Focus on Animal Models.Current topics in behavioral neurosciences · 2023Review
- Seminatural environments for rodent behavioral testing: a representative design improving animal welfare and enhancing replicability.Frontiers in behavioral neuroscience · 2023Article
- Social anhedonia as a Disrupted-in-Schizophrenia 1-dependent phenotype.Scientific reports · 2022Article
- Maternal Inflammation During Pregnancy and Offspring Brain Development: The Role of Mitochondria.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2022Review
- Presynaptic vesicular accumulation is required for antipsychotic efficacy in psychotic-like rats.Journal of psychopharmacology (Oxford, England) · 2021Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic pruning is a critical refinement step during neurodevelopment, and schizophrenia has been associated with overpruning of cortical dendritic spines. Both human studies and animal models implicate disrupted-in-schizophrenia 1 (DISC1) gene as a strong susceptibility factor for schizophrenia. Accumulating evidence supports the involvement of DISC1 protein in the modulation of synaptic elimination during critical periods of neurodevelopment and of dopamine D2-receptor-mediated signaling during adulthood. In many species, synaptic pruning occurs during juvenile and adolescent periods and is mediated by microglia, which can be over-activated by an immune challenge, giving rise to overpruning. Therefore, we sought to investigate possible interactions between a transgenic DISC1 model (tgDISC1) and juvenile immune activation (JIA) by the bacterial cell wall endotoxin lipopolysaccharide on the induction of schizophrenia-related behavioral and neurochemical disruptions in adult female and male rats. We examined possible behavioral aberrations along three major symptom dimensions of schizophrenia including psychosis, social and emotional disruptions, and cognitive impairments. We detected significant gene-environment interactions in the amphetamine-induced locomotion in female animals and in the amphetamine-induced anxiety in male animals. Surprisingly, gene-environment interactions improved social memory in both male and female animals. JIA alone disrupted spatial memory and recognition memory, but only in male animals. DISC1 overexpression alone induced an improvement in sensorimotor gating, but only in female animals. Our neurochemical analyses detected sex- and manipulation-dependent changes in the postmortem monoamine content of animals. Taken together, we here report sex-specific effects of environment and genotype as well as their interaction on behavioral phenotypes and neurochemical profiles relevant for schizophrenia.
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