Anxiety disorders are associated with a failure to sufficiently extinguish fear memories. The serotonergic system (5-hydroxytryptamine, 5-HT) with the 5-HT transporter (5-HTT, SERT) is strongly implicated in the regulation of anxiety and fear. In the present study, we examined the effects of SERT deficiency on fear extinction in a differential fear conditioning paradigm in male and female rats. Fear-related behavior displayed during acquisition, extinction, and recovery, was measured through quantification of immobility and alarm 22-kHz ultrasonic vocalizations (USV). Trait-like inter-individual differences in novelty-seeking, anxiety-related behavior, habituation learning, cognitive performance, and pain sensitivity were examined for their predictive value in forecasting fear extinction. Our results show that SERT deficiency strongly affected the emission of 22-kHz USV during differential fear conditioning. During acquisition, extinction, and recovery, SERT deficiency consistently led to a reduction in 22-kHz USV emission. While SERT deficiency did not affect immobility during acquisition, genotype differences started to emerge during extinction, and during recovery rats lacking SERT showed higher levels of immobility than wildtype littermate controls. Recovery was reflected in increased levels of immobility but not 22-kHz USV emission. Prominent sex differences were evident. Among several measures for trait-like inter-individual differences, anxiety-related behavior had the best predictive quality.
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http://dx.doi.org/10.3390/ijms22137088 | DOI Listing |
Front Biosci (Landmark Ed)
January 2025
Division of Molecular Psychiatry, Center of Mental Health, University of Hospital Würzburg, 97080 Würzburg, Germany.
Background: The inheritance of the short allele, encoding the serotonin transporter (SERT) in humans, increases susceptibility to neuropsychiatric and metabolic disorders, with aging and female sex further exacerbating these conditions. Both central and peripheral mechanisms of the compromised serotonin (5-HT) system play crucial roles in this context. Previous studies on SERT-deficient (Sert) mice, which model human SERT deficiency, have demonstrated emotional and metabolic disturbances, exacerbated by exposure to a high-fat Western diet (WD).
View Article and Find Full Text PDFJ Neuroimmune Pharmacol
September 2024
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Kasr El Aini St, Cairo, Egypt.
Cardiovasc Pathol
November 2024
Department of Surgery, Columbia University; New York, NY 10032, USA; Department of Biomedical Engineering, Columbia University, New York, NY 10027, USA. Electronic address:
BMC Med Inform Decis Mak
August 2024
Department of Business Administration (Quantitative Methods), Gaziantep University, Gaziantep, Turkey.
Background: To investigate how successfully the classification of patients with and without dental anomalies was achieved through four experiments involving different dental anomalies.
Methods: Lateral cephalometric radiographs (LCRs) from 526 individuals aged between 14 and 22 years were included. Four experiments involving different dental anomalies were created.
Biomolecules
July 2024
Department of Pharmacology, Oxford University, Oxford OX1 3QT, UK.
The impaired function of the serotonin transporter (SERT) in humans has been linked to a higher risk of obesity and type 2 diabetes, especially as people age. Consuming a "Western diet" (WD), which is high in saturated fats, cholesterol, and sugars, can induce metabolic syndrome. Previous research indicated that mice carrying a targeted inactivation of the gene (knockout, KO) and fed a WD display significant metabolic disturbances and behaviors reminiscent of ADHD.
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