Neuroscience
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Cell swelling usually initiates the regulatory volume decrease (RVD) process mediated mainly by volume-regulated anion channels (VRACs), which are formed by multiple different leucine-rich repeat-containing protein 8 (LRRC8) family members. VRAC currents have been widely recorded in astrocytes, neurons and microglia in the brain, and VRACs have been suggested to be involved in the important pathogenesis of cell swelling-related central nervous system (CNS) diseases, such as ischemic stroke, epilepsy and epileptogenesis, glioblastoma (GBM), and so on. ⋯ After cerebral ischemia, the swollen astrocytes, neurons and microglia can activate LRRC8A-dependent VRACs, which may respectively promote the release of excitatory amino acids (EAA), interaction with ionotropic glutamate receptors, and regulating inflammation, suggesting the pleiotropic roles of LRRC8A in swollen brain cells. For the treatment of cell swelling-related CNS diseases, specific targeting LRRC8A may be a superior strategy to inhibit swollen-induced VRAC hyperactivity without blocking the normal VRAC function.
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Randomized Controlled Trial
Strengthening the GABAergic System Through Neurofeedback Training Suppresses Implicit Motor Learning.
Gamma-aminobutyric acid (GABA) activity within the primary motor cortex (M1) is essential for motor learning in cortical plasticity, and a recent study has suggested that real-time neurofeedback training (NFT) can self-regulate GABA activity. Therefore, this study aimed to investigate the effect of GABA activity strengthening via NFT on subsequent motor learning. Thirty-six healthy participants were randomly assigned to either an NFT group or control group, which received sham feedback. ⋯ We measured the reaction time before, after (online learning), and 24 h after (offline learning) the finger-tapping task. Results showed the strengthening of GABA activity induced by the NFT intervention, and the suppression of the online but not the offline learning. These findings suggest that prior GABA activity modulation may affect online motor learning.
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Chronic macrophage activation was implicated as one of the main culprits for chronical, low-grade inflammation which significantly contributes to development of age-related diseases. Microglia as the brain macrophages have been recently implicated as key players in neuroinflammation and neurodegeneration in the aged brain. Microglial cell functions are indispensable in early development, however, activation or senescence of microglia in aging cells may be detrimental. ⋯ By using low doses we could achieve reduction in inflammation circumventing the astrocyte activation. Removal of microglia cells led to decreased expression of the senescence marker p16Ink4a in the aged brain, indicating a relevant contribution of these cells to the expression of this marker and their senescent status in the healthy aging brain. Our results indicate that increased and detrimental brain inflammation in aged murine brain can be impaired by selectively reducing the microglial cell population.
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Within the nervous system, plasticity mechanisms attempt to stabilize network activity following disruption by injury, disease, or degeneration. Optic nerve injury and age-related diseases can induce homeostatic-like responses in adulthood. We tested this possibility in the thalamocortical (TC) neurons in the dorsolateral geniculate nucleus (dLGN) using patch-clamp electrophysiology, optogenetics, immunostaining, and single-cell dendritic analysis following loss of visual input via bilateral enucleation. ⋯ Analysis of TC neuron dendritic structure from single-cell dye fills revealed a gradual loss of dendrites proximal to the soma, where TC neurons receive the bulk of RG inputs. Finally, analysis of action potential firing demonstrated that TC neurons have increased excitability following enucleation, firing more action potentials in response to depolarizing current injections. Our findings show that degeneration of the retinal axons/optic nerve and loss of RG synaptic inputs induces structural and functional changes in TC neurons, consistent with neuronal attempts at compensatory plasticity in the dLGN.
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Adverse effects of changing climate have been associated with increase average global temperature resulting in environmental changes. We set out to investigate effects of environmental stress due to increased heat exposure on developmental milestones, behaviour, gut microbiota and neuroarchitecture in rat pups. Pregnant Wistar rats were held in standard temperature (ST) (26 ± 2 °C; control) or high temperature (HT) (40 ± 2 °C) housing. ⋯ There was also a reduction in MBP expression in the HT pups. Taken together, our results revealed a delay in neurodevelopmental milestones in pups exposed to high HT during gestation and post natal life. Pups whose dam were exposed to high HT during gestation also showed some set back but improved over the course of testing.