78 results found
    1. Neuroscience

    Alzheimer’s disease risk gene BIN1 induces Tau-dependent network hyperexcitability

    Yuliya Voskobiynyk et al.
    BIN1 forms a complex with Tau and voltage-gated calcium channels in neurons, and higher BIN1 levels promote neuronal activity, calcium influx, and bursting that is blocked by reducing Tau.
    1. Neuroscience

    Early intrinsic hyperexcitability does not contribute to motoneuron degeneration in amyotrophic lateral sclerosis

    Félix Leroy et al.
    Contrary to a long-standing hypothesis, the neuronal death that leads to muscle wastage in amyotrophic lateral sclerosis does not result from overactivity of those neurons during development.
    1. Neuroscience

    Mechanisms of hyperexcitability in Alzheimer’s disease hiPSC-derived neurons and cerebral organoids vs isogenic controls

    Swagata Ghatak et al.
    Increased excitation and decreased inhibition associated with abnormal neuronal morphology, aberrant ion channel properties, and synaptic dysfunction contribute to hyperexcitability in Alzheimer’s disease hiPSC-derived neuronal cultures and cerebral organoids.
    1. Neuroscience

    Hypoexcitability precedes denervation in the large fast-contracting motor units in two unrelated mouse models of ALS

    María de Lourdes Martínez-Silva et al.
    The most vulnerable motor units lose a fundamental firing property before the denervation of their muscle fibers in ALS mice, changing our view of the role of excitability in neurodegeneration.
    1. Microbiology and Infectious Disease
    2. Neuroscience

    Neuronal hyperexcitability is a DLK-dependent trigger of herpes simplex virus reactivation that can be induced by IL-1

    Sean R Cuddy et al.
    Herpes simplex virus reactivates from a latent infection when neurons become hyperexcitable in response to an inflammatory cytokine known to be released during fever and stress.
    1. Neuroscience

    Calpain fosters the hyperexcitability of motoneurons after spinal cord injury and leads to spasticity

    Vanessa Plantier et al.
    Calpain is a promising therapeutic target to reduce spasticity after a spinal cord injury.
    1. Neuroscience

    Altered potassium channel distribution and composition in myelinated axons suppresses hyperexcitability following injury

    Margarita Calvo et al.
    Type 1 potassium channels alter their composition and localisation to suppress hyper-excitability and neuropathic pain of injured sensory neurons.
    1. Neuroscience

    Criticality and degeneracy in injury-induced changes in primary afferent excitability and the implications for neuropathic pain

    Stéphanie Ratté et al.
    No single molecular change is uniquely necessary to cause neuropathic changes in primary afferent excitability; multiple different changes are sufficient.
    1. Neuroscience

    Stxbp1/Munc18-1 haploinsufficiency impairs inhibition and mediates key neurological features of STXBP1 encephalopathy

    Wu Chen et al.
    Two genetically distinct Stxbp1 haploinsufficiency mouse models exhibit seizures and impairments in cognitive, psychiatric, and motor functions, representing robust preclinical models of STXBP1 encephalopathy with both construct and face validity.
    1. Cell Biology
    2. Neuroscience

    Bidirectional regulation of glial potassium buffering – glioprotection versus neuroprotection

    Hailun Li et al.
    A neuromodulatory circuit bidirectionally regulates the glial capacity to buffer ions and water in response to changes in neuronal excitation in order to balance glial versus neuronal protection.

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