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Fragile X syndrome (FXS) is the most common inherited cause of intellectual disability and is the leading known single-gene cause of autism spectrum disorder. Patients with FXS display varied behavioural deficits that include mild to severe cognitive impairments in addition to mood disorders. Currently, there is no cure for this condition; however, there is an emerging focus on therapies that inhibit mechanistic target of rapamycin (mTOR)-dependent protein synthesis owing to the clinical effectiveness of metformin for alleviating some behavioural symptoms in FXS. Adiponectin (APN) is a neurohormone that is released by adipocytes and provides an alternative means to inhibit mTOR activation in the brain. In these studies, we show that knockout mice, like patients with FXS, show reduced levels of circulating APN and that both long-term potentiation (LTP) and long-term depression (LTD) in the dentate gyrus (DG) are impaired. Brief (20 min) incubation of hippocampal slices in APN (50 nM) was able to rescue both LTP and LTD in the DG and increased both the surface expression and phosphorylation of GluA1 receptors. These results provide evidence for reduced APN levels in FXS playing a role in decreasing bidirectional synaptic plasticity and show that therapies which enhance APN levels may have therapeutic potential for this and related conditions.This article is part of a discussion meeting issue 'Long-term potentiation: 50 years on'.
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http://dx.doi.org/10.1098/rstb.2023.0221 | DOI Listing |
Hum Brain Mapp
December 2024
Institute of Cognitive Neuroscience, Department of Biopsychology, Faculty of Psychology, Ruhr University Bochum, Bochum, Germany.
Learning new categories is fundamental to cognition, occurring in daily life through various sensory modalities. However, it is not well known how acquiring new categories can modulate the brain networks. Resting-state functional connectivity is an effective method for detecting short-term brain alterations induced by various modality-based learning experiences.
View Article and Find Full Text PDFPsychedelic Med (New Rochelle)
December 2024
Departments of Anesthesiology and Critical Care, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Introduction: Psychedelic-induced experiences are thought to play an important role in the therapeutic actions of rapid-acting antidepressants. General anesthesia is one scenario in which patients can be rendered unconscious and masked to the psychedelic treatment, providing a simple yet effective method to examine drug-induced changes in the brain devoid of experiences.
Methods: Chronically stressed adult C57/BL6 male mice were given subhypnotic ketamine alone or ketamine and GABAergic anesthetic isoflurane at sedative (0.
Front Neural Circuits
December 2024
Department of Physiology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
[This corrects the article DOI: 10.3389/fncir.2024.
View Article and Find Full Text PDFBiol Psychiatry Glob Open Sci
January 2025
Department of Psychiatry, New York University Grossman School of Medicine, New York, New York.
Background: An excess of exosomes, nanovesicles released from all cells and key regulators of brain plasticity, is an emerging therapeutic target for stress-related mental illnesses. The effects of chronic stress on exosome levels are unknown; even less is known about molecular drivers of exosome levels in the stress response.
Methods: We used our state-of-the-art protocol with 2 complementary strategies to isolate neuronal exosomes from plasma, ventral dentate gyrus, basolateral amygdala, and olfactory bulbs of male mice to determine the effects of chronic restraint stress (CRS) on exosome levels.
Exp Neurol
December 2024
Department of Neurology, Henry Ford Health System, Detroit, MI 48202, United States of America. Electronic address:
Dendritic and axonal plasticity, which mediates neurobiological recovery after a stroke, critically depends on the mitochondrial function of neurons. To investigate, in vivo, neuronal mitochondrial function at the stroke recovery stage, we employed Mito-tag mice combined with cerebral cortical infection of AAV9 produced from plasmids carrying Cre-recombinase controlled by two neuronal promoters, synapsin-I (SYN1) and calmodulin-kinase IIa to induce expression of a hemagglutinin (HA)-tagged enhanced green fluorescence protein (EGFP) that localizes to mitochondrial outer membranes of SYN1 positive (SYN) and CaMKIIa positive (CaMKIIa) neurons. These mice were then subjected to permanent middle cerebral artery occlusion (MCAO) and sacrificed 14 days post stroke.
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