ArticleThe Journal of biological chemistry2015
Prion Protein Modulates Monoaminergic Systems and Depressive-like Behavior in Mice.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Neonatal maternal separation causes depressive-like behavior and potentiates memory impairment induced by amyloid-β oligomers in adult mice.Behavioral and brain functions : BBF · 2025Article
- The prion protein is required for normal responses to light stimuli by photoreceptors and bipolar cells.iScience · 2024Article
- New Light on Prions: Putative Role of PrPInternational journal of molecular sciences · 2024Review
- Comorbidity between Alzheimer's disease and major depression: a behavioural and transcriptomic characterization study in mice.Alzheimer's research & therapy · 2021Article
- Treatment Response Biomarkers in Anxiety Disorders: From Neuroimaging to Neuronally-Derived Extracellular Vesicles and Beyond.Biomarkers in neuropsychiatry · 2020Article
- The Role of the Mammalian Prion Protein in the Control of Sleep.Pathogens (Basel, Switzerland) · 2017Review
- LPS-induced systemic inflammation reveals an immunomodulatory role for the prion protein at the blood-brain interface.Journal of neuroinflammation · 2017Article
- Expression of Tyrosine Hydroxylase is Negatively Regulated Via Prion Protein.Neurochemical research · 2016Article
- Article
- Functions of the cellular prion protein, the end of Moore's law, and Ockham's razor theory.Prion · 2016Article
- Review
- Altered Monoaminergic Systems and Depressive-like Behavior in Congenic Prion Protein Knock-out Mice.The Journal of biological chemistry · 2015Article
- Reply to Altered Monoaminergic Systems and Depressive-like Behavior in Congenic Prion Protein Knock-out Mice.The Journal of biological chemistry · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We sought to examine interactions of the prion protein (PrP(C)) with monoaminergic systems due to: the role of PrP(C) in both Prion and Alzheimer diseases, which include clinical depression among their symptoms, the implication of monoamines in depression, and the hypothesis that PrP(C) serves as a scaffold for signaling systems. To that effect we compared both behavior and monoaminergic markers in wild type (WT) and PrP(C)-null (PrP(-/-)) mice. PrP(-/-) mice performed poorly when compared with WT in forced swimming, tail suspension, and novelty suppressed feeding tests, typical of depressive-like behavior, but not in the control open field nor rotarod motor tests; cyclic AMP responses to stimulation of D1 receptors by dopamine was selectively impaired in PrP(-/-) mice, and responses to serotonin, but not to norepinephrine, also differed between genotypes. Contents of dopamine, tyrosine hydroxylase, and the 5-HT5A serotonin receptor were increased in the cerebral cortex of PrP(-/-), as compared with WT mice. Microscopic colocalization, as well as binding in overlay assays were found of PrP(C) with both the 5HT5A and D1, but not D4 receptors. The data are consistent with the scaffolding of monoaminergic signaling modules by PrP(C), and may help understand the pathogenesis of clinical depression and neurodegenerative disorders.
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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.