ArticleFrontiers in cellular neuroscience2020
Acute Pannexin 1 Blockade Mitigates Early Synaptic Plasticity Defects in a Mouse Model of Alzheimer's Disease.
Article in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 33 citations in OpenAlex.
- Panx1a modulates metabolic stress signaling and synaptic composition in the developing zebrafish brain.Cell and tissue research · 2025Article
- Dual role for pannexin 1 at synapses: regulating functional and morphological plasticity.The Journal of physiology · 2025Review
- Serum levels of neurotensin, pannexin-1, and sestrin-2 and the correlations with sleep quality or/and cognitive function in the patients with chronic insomnia disorder.Frontiers in psychiatry · 2024Article
- Overlap in synaptic neurological condition susceptibility pathways and the neural pannexin 1 interactome revealed by bioinformatics analyses.Channels (Austin, Tex.) · 2023Article
- Probenecid, an Old Drug with Potential New Uses for Central Nervous System Disorders and Neuroinflammation.Biomedicines · 2023Review
- The Long-Term Pannexin 1 Ablation Produces Structural and Functional Modifications in Hippocampal Neurons.Cells · 2022Article
- Connexins and Pannexins: Important Players in Neurodevelopment, Neurological Diseases, and Potential Therapeutics.Biomedicines · 2022Review
- ER-resident STIM1/2 couples CaProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Delivering the Promise of Gene Therapy with Nanomedicines in Treating Central Nervous System Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Review
- Altered Metabolism in Alzheimer Disease Brain: Role of Oxidative Stress.Antioxidants & redox signaling · 2022Review
- SIRT1 Is Involved in the Neuroprotection of Pterostilbene Against Amyloid β 25-35-Induced Cognitive Deficits in Mice.Frontiers in pharmacology · 2022Article
- Pannexin 1 channels and ATP release in epilepsy: two sides of the same coin : The contribution of pannexin-1, connexins, and CALHM ATP-release channels to purinergic signaling.Purinergic signalling · 2021Review
- The biological pathways of Alzheimer disease: a review.AIMS neuroscience · 2021Review
- Absence of Pannexin 1 Stabilizes Hippocampal Excitability After Intracerebral Treatment With Aβ (1-42) and Prevents LTP Deficits in Middle-Aged Mice.Frontiers in aging neuroscience · 2021Article
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12 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Synaptic loss induced by soluble oligomeric forms of the amyloid β peptide (sAβos) is one of the earliest events in Alzheimer's disease (AD) and is thought to be the major cause of the cognitive deficits. These abnormalities rely on defects in synaptic plasticity, a series of events manifested as activity-dependent modifications in synaptic structure and function. It has been reported that pannexin 1 (Panx1), a nonselective channel implicated in cell communication and intracellular signaling, modulates the induction of excitatory synaptic plasticity under physiological contexts and contributes to neuronal death under inflammatory conditions. Here, we decided to study the involvement of Panx1 in functional and structural defects observed in excitatory synapses of the amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic (Tg) mice, an animal model of AD. We found an age-dependent increase in the Panx1 expression that correlates with increased Aβ levels in hippocampal tissue from Tg mice. Congruently, we also observed an exacerbated Panx1 activity upon basal conditions and in response to glutamate receptor activation. The acute inhibition of Panx1 activity with the drug probenecid (PBN) did not change neurodegenerative parameters such as amyloid deposition or astrogliosis, but it significantly reduced excitatory synaptic defects in the AD model by normalizing long-term potentiation (LTP) and depression and improving dendritic arborization and spine density in hippocampal neurons of the Tg mice. These results suggest a major contribution of Panx1 in the early mechanisms leading to the synaptopathy in AD. Indeed, PBN induced a reduction in the activation of p38 mitogen-activated protein kinase (MAPK), a kinase widely implicated in the early neurotoxic signaling in AD. Our data strongly suggest that an enhanced expression and activation of Panx1 channels contribute to the Aβ-induced cascades leading to synaptic dysfunction in AD.
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