Neuroscience
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Cerebral ischemic/reperfusion (I/R) injury has high disability and morbidity. Hypoxia-inducible factor-1α (HIF-1α) may enhance the transcriptional activity of transferrin ferroportin 1 (FPN1) in regulating ferroptosis after cerebral ischemia injury (CII). In this study, cerebral I/R injury rat models were established and treated with pcDNA3.1-HIF-1α, pcDNA3.1-NC lentiviral plasmid, or ML385 (a specific Nrf2 inhibitor). ⋯ FPN1 knockdown reversed HIF-1α-mediated alleviation of OGD/R-induced ferroptosis. HIF-1α activated the Nrf2/HO-1 pathway by enhancing FPN1 expression and alleviating OGD/R-induced ferroptosis. Conjointly, HIF-1α enhanced the transcriptional activity of FPN1, activated the Nrf2/HO-1 pathway, and inhibited ferroptosis of brain neurons, thereby improving I/R injury in CII rats.
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There are currently no pharmacological treatments for cocaine use disorder. Recently there has been a great deal of interest in the potential of psychedelic drugs such as psilocybin to treat psychiatric disorders. Human studies have indicated that a single administration of psilocybin can have long-lasting effects. ⋯ Psilocybin administered following extinction trials had no effect, as both female and male mice and rats demonstrated significant cue-induced reinstatement. These data suggest that psilocybin is ineffective at altering cocaine-seeking behavior in the paradigm and doses used in the current study. It remains to be seen whether treatment with psilocybin under different conditions may be useful in the long-standing goal of finding pharmacotherapies to treat CUD.
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Philippe Ascher spent his last two decades as an emeritus Professor, working in the heart of Paris. Together with his wife Jacsue they were hosted in Alain Marty's laboratory and enjoyed the happiest retirement. ⋯ This period led us from NMDA receptors to the corelease of acetylcholine and glutamate by spinal motoneurons to Renshaw cells and then to the stoichiometric variants of nicotinic acetylcholine receptors. Here I present a brief history of our collaboration during this period.
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Fluorosis is a global public health concern. Prolonged exposure to excessive fluoride causes fluoride accumulation in the hippocampus, resulting in cognitive dysfunction. Cell death is necessary for maintaining tissue function and morphology, and changes in the external morphology of nerve cells and the function of many internal organelles are typical features of cell death; however, it is also a typical feature of cognitive impairment caused by fluorosis. ⋯ Herein, we provide an overview of cognitive impairment caused by excessive fluoride exposure in different age groups, and the underlying mechanisms for cognitive impairment in various model organisms. The mechanisms underlying these impairments include oxidative stress, synaptic and neurotransmission dysfunction, disruption of mitochondrial and energy metabolism, and calcium channel dysregulation. This study aims to provide potential insights that serve as a reference for subsequent research on the cognitive function caused by excessive fluoride.