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Oxytocin (OT) orchestrates social and emotional behaviors through modulation of neural circuits. In the central amygdala, the release of OT modulates inhibitory circuits and, thereby, suppresses fear responses and decreases anxiety levels. Using astrocyte-specific gain and loss of function and pharmacological approaches, we demonstrate that a morphologically distinct subpopulation of astrocytes expresses OT receptors and mediates anxiolytic and positive reinforcement effects of OT in the central amygdala of mice and rats. The involvement of astrocytes in OT signaling challenges the long-held dogma that OT acts exclusively on neurons and highlights astrocytes as essential components for modulation of emotional states under normal and chronic pain conditions.
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http://dx.doi.org/10.1038/s41593-021-00800-0 | DOI Listing |
Brain Behav Immun
September 2025
Department of Behavioral and Molecular Neurobiology, University of Regensburg, Regensburg, Germany. Electronic address:
Chronic psychosocial stress is a frequent burden in modern societies and risk factor for numerous somatic and affective disorders, including social anxiety disorder (SAD). Traumatic experiences after prolonged periods of stress exposure often trigger these diseases. Although human and animal studies support the hypothesis of an over-reactive immune system being critically involved in the pathogenesis of psychopathologies, the underlying mechanisms are not fully understood.
View Article and Find Full Text PDFJ Neurosci
September 2025
Center for Studies in Behavioural Neurobiology, Department of Psychology, Concordia University, Montreal, QC, Canada, H4B 1R6
Adaptive behavior depends on a dynamic balance between acquisition and extinction memories. Male and female rodents differ in extinction learning rates, suggestion potential sex-based differences in this balance. In males, deletion of extinction-recruited neurons in the central nucleus (CN) of the amygdala impairs extinction retrieval, shifting behavior toward acquisition (Lay et al.
View Article and Find Full Text PDFPLoS One
September 2025
Escuela Nacional de Estudios Superiores Unidad Juriquilla, Campus UNAM-Juriquilla, Universidad Nacional Autónoma de México, Querétaro, Querétaro, Mexico.
In the adult brain, neurogenesis primarily occurs in the dentate gyrus of the hippocampus (DG) and the olfactory bulbs, with new cells migrating from the subventricular zone. Additionally, small amounts of cell proliferation have been observed in the preoptic area (POA) and the amygdala (AMG), regions involved in the control of male sexual behavior. Sexual activity induces a reward state mediated by opioids, and our group previously demonstrated that neurogenesis induced by paced mating is opioid dependent in female rats.
View Article and Find Full Text PDFNeuroimage Rep
September 2025
Department of Endocrinology, Amsterdam University Medical Centers, location VUMC, Amsterdam, the Netherlands.
People with obesity tend to have altered functional connectivity of reward-related areas in the brain, contributing to overeating and weight gain. The gut-brain axis may function as a mediating factor, with gut-derived short-chain fatty acids (SCFAs) as possible intermediates in the relationship between microbiota and functional connectivity. We investigated the influence of SCFA turnover on resting state functional connectivity in healthy individuals with extremely high and extremely low levels of intestinal SCFA turnover.
View Article and Find Full Text PDF3 Biotech
September 2025
Department of Anatomy, Kasturba Medical College Mangalore, Manipal Academy of Higher Education, Manipal, India.
Neuroinflammation is known to be a contributing factor for several neurological disorders as well as cognitive dysfunction. Different signalling pathways, and a variety of supporting cells of CNS are suggested to be involved in the progression of neurodegeneration. Among the factors contributing to neuroinflammation, peripheral inflammation takes a lead role according to recent research, since persistent peripheral inflammation is believed to disrupt the blood-brain barrier (BBB).
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