ArticleTranslational psychiatry2019
Deletion of Dtnbp1 in mice impairs threat memory consolidation and is associated with enhanced inhibitory drive in the amygdala.
Article in Translational psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Sex dimorphism controls dysbindin-related cognitive dysfunctions in mice and humans with the contribution of COMT.Molecular psychiatry · 2024Article
- Transcriptomics analysis reveals potential regulatory role of nSMase2 (Smpd3) in nervous system development and function of middle-aged mouse brains.Genes, brain, and behavior · 2024Article
- Dysbindin-1, BDNF, and GABAergic Transmission in Schizophrenia.Frontiers in psychiatry · 2022Review
- Synapse-specific roles for microglia in development: New horizons in the prefrontal cortex.Frontiers in molecular neuroscience · 2022Review
- Article
- Loss of dysbindin-1 affects GABAergic transmission in the PFC.Psychopharmacology · 2019Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Schizophrenia is a severe and highly heritable disorder. Dystrobrevin-binding protein 1 (DTNBP1), also known as dysbindin-1, has been implicated in the pathophysiology of schizophrenia. Specifically, dysbindin-1 mRNA and protein expression are decreased in the brains of subjects with this disorder. Mice lacking dysbinidn-1 also display behavioral phenotypes similar to those observed in schizophrenic patients. However, it remains unknown whether deletion of dysbindin-1 impacts functions of the amygdala, a brain region that is critical for emotional processing, which is disrupted in patients with schizophrenia. Here, we show that dysbindin-1 is expressed in both excitatory and inhibitory neurons of the basolateral amygdala (BLA). Deletion of dysbindin-1 in male mice (Dys
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