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Deficits in social interaction or social cognition are key phenotypes in a variety of chronic mental diseases, yet, their modeling and molecular dissection are only in their infancy. The Disrupted-in-Schizophrenia 1 (DISC1) signaling pathway is considered to play a role in different psychiatric disorders such as schizophrenia, depression, and biopolar disorders. DISC1 is involved in regulating the dopaminergic neurotransmission in, among others, the mesolimbic reward system. A transgenic rat line tgDISC1 has been introduced as a model system to study behavioral phenotypes associated with abnormal DISC1 signaling pathways. Here, we evaluated the impact of impaired DISC1 signaling on social (social interaction) and non-social (sucrose) reward preferences in the tgDISC1 animal model. In a plus-maze setting, rats chose between the opportunity for social interaction with an unfamiliar juvenile conspecific (social reward) or drinking sweet solutions with variable sucrose concentrations (non-social reward). tgDISC1 rats differed from wild-type rats in their social, but not in their non-social reward preferences. Specifically, DISC1 rats showed a lower interest in interaction with the juvenile conspecific, but did not differ from wild-type rats in their preference for higher sucrose concentrations. These results suggest that disruptions of the DISC1 signaling pathway that is associated with altered dopamine transmission in the brain result in selective deficits in social motivation reminiscent of phenotypes seen in neuropsychiatric illness.
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http://dx.doi.org/10.1038/s41598-022-14102-3 | DOI Listing |
Biochem Biophys Res Commun
January 2025
College of Pharmacy, Chung-Ang University, Seoul 06974, Republic of Korea. Electronic address:
Radiation therapy represents the primary treatment option for triple-negative breast cancer. However, radio resistance is associated with a poor prognosis and an increased risk of recurrence. Radioresistant MDA-MB-231 cells, a radioresistant triple-negative breast cancer cell line, were co-treated with ortho-topolin riboside and melatonin.
View Article and Find Full Text PDFDev Neurosci
October 2024
The Department of Clinical Laboratory, The 4th Affiliated Hospital of Harbin Medical University, Harbin, China.
Introduction: Sevoflurane is an extensively used anesthetic for pediatric patients; however, numerous studies showed that sevoflurane (SEVO) may cause long-term neurodevelopmental toxicity. Dexmedetomidine (DEX) has been shown to be protective against SEVO-induced neurotoxicity, but the mechanism remains unclear. The effects and mechanisms of different DEX administration routes on SEVO-induced neurotoxicity and long-term cognitive defects were determined and further investigated the role of sex in these processes.
View Article and Find Full Text PDFInt J Mol Sci
May 2024
Department of Neurology, Medical University of Warsaw, 02-091 Warsaw, Poland.
Gilles de la Tourette syndrome (GTS) is a neurodevelopmental psychiatric disorder with complex and elusive etiology with a significant role of genetic factors. The aim of this study was to identify structural variants that could be associated with familial GTS. The study group comprised 17 multiplex families with 80 patients.
View Article and Find Full Text PDFFront Mol Neurosci
May 2024
Department of Anesthesiology, Perioperative and Pain Medicine, Boston Children's Hospital, Boston, MA, United States.
Introduction: Disrupted in schizophrenia-1 (DISC1) is a scaffolding protein whose mutated form has been linked to schizophrenia, bipolar affective disorders, and recurrent major depression. DISC1 regulates multiple signaling pathways involved in neurite outgrowth and cortical development and binds directly to glycogen synthase kinase-3β (GSK-3β). Since ketamine activates GSK-3β, we examined the impact of ketamine on DISC1 and GSK-3β expression.
View Article and Find Full Text PDFBMC Neurosci
March 2024
Department of Pharma and Biotech, NMI Natural and Medical Sciences Institute at the University of Tübingen, 72770, Reutlingen, Germany.
Background: Mutations in the gene DISC1 are associated with increased risk for schizophrenia, bipolar disorder and major depression. The study of mutated DISC1 represents a well-known and comprehensively characterized approach to understand neuropsychiatric disease mechanisms. However, previous studies have mainly used animal models or rather heterogeneous populations of iPSC-derived neurons, generated by undirected differentiation, to study the effects of DISC1 disruption.
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