ArticleMolecular autism2018
17-β estradiol increases parvalbumin levels in
Article in Molecular autism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Gephyrin phosphorylation facilitates sexually dimorphic development and function of parvalbumin interneurons in the mouse hippocampus.Molecular psychiatry · 2024Article
- Role of estrogen in sex differences in memory, emotion and neuropsychiatric disorders.Molecular biology reports · 2024Review
- Circuit-level theories for sensory dysfunction in autism: convergence across mouse models.Frontiers in neurology · 2023Review
- GABA System Modifications During Periods of Hormonal Flux Across the Female Lifespan.Frontiers in behavioral neuroscience · 2022Review
- Age- and sex-specific effects of stress on parvalbumin interneurons in preclinical models: Relevance to sex differences in clinical neuropsychiatric and neurodevelopmental disorders.Neuroscience and biobehavioral reviews · 2021Review
- Sex Differences in Affective Dysfunction and Alterations in Parvalbumin in Rodent Models of Early Life Adversity.Frontiers in behavioral neuroscience · 2021Review
- The Role of Parvalbumin Interneurons in Neurotransmitter Balance and Neurological Disease.Frontiers in psychiatry · 2021Review
- Drug repositioning based on network-specific core genes identifies potential drugs for the treatment of autism spectrum disorder in children.Computational and structural biotechnology journal · 2021Article
- Article
- Cytosolic CaCold Spring Harbor perspectives in biology · 2020Review
- Neural Mechanisms Underlying Repetitive Behaviors in Rodent Models of Autism Spectrum Disorders.Frontiers in cellular neuroscience · 2020Review
- Parvalbumin-Deficiency Accelerates the Age-Dependent ROS Production in Pvalb NeuronsFrontiers in cellular neuroscience · 2020Article
- The Parvalbumin Hypothesis of Autism Spectrum Disorder.Frontiers in cellular neuroscience · 2020Article
- The Neuroprotective Effects of 17β-Estradiol Pretreatment in a Model of Neonatal Hippocampal Injury Induced by Trimethyltin.Frontiers in cellular neuroscience · 2018Article
- Dysregulation of Parvalbumin Expression in theFrontiers in molecular neuroscience · 2018Article
- Shank2 Deletion in Parvalbumin Neurons Leads to Moderate Hyperactivity, Enhanced Self-Grooming and Suppressed Seizure Susceptibility in Mice.Frontiers in molecular neuroscience · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by two core symptoms: impaired social interaction and communication, and restricted, repetitive behaviors and interests. The pathophysiology of ASD is not yet fully understood, due to a plethora of genetic and environmental risk factors that might be associated with or causal for ASD. Recent findings suggest that one putative convergent pathway for some forms of ASD might be the downregulation of the calcium-binding protein parvalbumin (PV). PV-deficient mice (PV-/-, PV+/-), as well as Shank1-/-, Shank3-/-, and VPA mice, which show behavioral deficits relevant to all human ASD core symptoms, are all characterized by lower PV expression levels. Methods: Based on the hypothesis that PV expression might be increased by 17-β estradiol (E2), PV+/- mice were treated with E2 from postnatal days 5-15 and ASD-related behavior was tested between postnatal days 25 and 31. Results: PV expression levels were significantly increased after E2 treatment and, concomitantly, sociability deficits in PV+/- mice in the direct reciprocal social interaction and the 3-chamber social approach assay, as well as repetitive behaviors, were attenuated. E2 treatment of PV+/+ mice did not increase PV levels and had detrimental effects on sociability and repetitive behavior. In PV-/- mice, E2 obviously did not affect PV levels; tested behaviors were not different from the ones in vehicle-treated PV-/- mice. Conclusion: Our results suggest that the E2-linked amelioration of ASD-like behaviors is specifically occurring in PV+/- mice, indicating that PV upregulation is required for the E2-mediated rescue of ASD-relevant behavioral impairments.
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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.