Neuroscience
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Intestinal immunity is associated with several autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and type 1 diabetes. Recent evidence also suggests its implication in the pathogenesis of autoimmune diseases affecting the central nervous system, such as multiple sclerosis (MS). However, there is ongoing debate regarding which part of the intestinal tract contributes to the development of MS. ⋯ Additionally, we highlighted an increase in dendritic cells and monocytes/macrophages in the colonic lamina propria of EAE animals during the presymptomatic phase. Altogether, our findings indicate that both small intestine and colon are involved in the pathogenesis of EAE, despite engaging distinct immunological processes. This study provides new insights for understanding the roles of intestinal lymphoid and myeloid immune cells on the pathogenesis of MS and other autoimmune diseases.
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Exercise-induced fatigue (EF) is characterized by a decline in maximal voluntary muscle force following prolonged physical activity, influenced by both peripheral and central factors. Central fatigue involves complex interactions within the central nervous system (CNS), where astrocytes play a crucial role. This study explores the impact of astrocytic calcium signals on EF. ⋯ Utilizing genetic tools to either enhance or reduce astrocytic calcium signaling, we observed corresponding decreases and increases in exercise-induced fatigue time, respectively. Furthermore, modulation of astrocytic calcium signals influenced corticostriatal synaptic plasticity, with increased signals impairing and decreased signals ameliorating long-term depression (LTD). These results highlight the pivotal role of astrocytic calcium signaling in the regulation of exercise-induced fatigue and synaptic plasticity in the striatum.
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This study aims to delve into the mechanisms underlying the improvement of neurological function in rats with ischemic stroke through fecal microbiota transplantation. ⋯ Fecal microbiota transplantation offers a promising approach to improving neurological function in rats with ischemic stroke by inhibiting neuronal apoptosis, necroptosis, and the polarization of inflammatory microglial cells.
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Pain and itch are unpleasant and distinct sensations that give rise to behaviors such as reflexive withdrawal and scratching in humans and mice. Interestingly, it has been observed that pain modulates itch through the neural circuits housed in the brain and spinal cord. However, we have yet to fully understand the identities and mechanisms by which specific neural circuits mediate pain-induced modulation of itch. ⋯ The RVMTacr1 neurons were found to be nociceptive, sufficient for inhibiting itch, and necessary for pain-induced itch suppression. Moreover, through brain-wide anterograde and retrograde viral tracing studies, we found that the RVMTacr1 neurons are bidirectionally connected with LPBN, periaqueductal gray (PAG), and lateral hypothalamic area (LHA). Thus, together, our data indicate that the RVMTacr1 neurons integrate nociceptive information to mediate itch-induced scratching and can mediate the physiological effects of itch through their downstream targets.
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Cocaine abstinence and withdrawal are linked to relapse and heightened anxiety. While L-type calcium channels (LTCCs) have been associated with cocaine use disorders in humans and drug-seeking in rodents, their role in mood-related symptoms during cocaine abstinence remains unclear. We addressed this by investigating the ability of LTCC blockade with isradipine to alter the mood-related behavioral phenotypes induced by cocaine abstinence. ⋯ In contrast 1.2 mg/kg, i.p. isradipine decreased immobility time in both cocaine and saline abstinent female and male rats. In summary, isradipine administration reversed the anxiogenic and increased the FST immobility time associated with cocaine abstinence in a dose and sex-dependent manner. The data underscore the importance of further investigation of LTCC mechanisms and their therapeutic potential for mood disorders associated with cocaine use disorder.