ArticleNeurochemical research2012
Pannexin1-mediated ATP release provides signal transmission between Neuro2A cells.
Article in Neurochemical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Dual Regulatory Roles of Pannexin 1 in the Pathogenesis and Recovery of Sepsis-Induced Acute Lung Injury.Infection and drug resistance · 2025Review
- Neuronal Panx1 drives peripheral sensitization in experimental plantar inflammatory pain.Military Medical Research · 2024Article
- Article
- Human Pannexin 1 channel: Insight in structure-function mechanism and its potential physiological roles.Molecular and cellular biochemistry · 2021Review
- Pannexin 1 Regulates Skeletal Muscle Regeneration by Promoting Bleb-Based Myoblast Migration and Fusion Through a Novel Lipid Based Signaling Mechanism.Frontiers in cell and developmental biology · 2021Article
- Protective Effects of Hydrogen Sulfide Against the ATP-Induced Meningeal Nociception.Frontiers in cellular neuroscience · 2020Article
- Potential role for a specialized βJournal of orthopaedic research : official publication of the Orthopaedic Research Society · 2018Article
- Imaging extracellular ATP with a genetically-encoded, ratiometric fluorescent sensor.PloS one · 2017Article
- Clusters of specialized detector cells provide sensitive and high fidelity receptor signaling in the intact endothelium.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Suramin inhibits cell proliferation in ovarian and cervical cancer by downregulating heparanase expression.Cancer cell international · 2015Article
- Hypoxia-induced changes in Ca(2+) mobilization and protein phosphorylation implicated in impaired wound healing.American journal of physiology. Cell physiology · 2014Article
- Molecular pathways of pannexin1-mediated neurotoxicity.Frontiers in physiology · 2014Review
- Possible role of hemichannels in cancer.Frontiers in physiology · 2014Article
- The pannexins: past and present.Frontiers in physiology · 2014Review
- Relevance of gap junctions and large pore channels in traumatic brain injury.Frontiers in physiology · 2014Review
- Connexin and pannexin hemichannels in brain glial cells: properties, pharmacology, and roles.Frontiers in pharmacology · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Pannexin1 (Panx1), a protein related to the gap junction proteins of invertebrates, forms nonjunctional channels that open upon depolarization and in response to mechanical stretch and purinergic receptor stimulation. Importantly, ATP can be released through Panx1 channels, providing a possible role for these channels in non-vesicular signal transmission. In this study we expressed exogenous human and mouse Panx1 in the gap junction deficient Neuro2A neuroblastoma cell line and explored the contribution of Panx1 channels to cell-cell communication as sites of ATP release. Electrophysiological (patch clamp) recordings from Panx1 transfected Neuro2A cells revealed membrane conductance that increased beyond 0 mV when applying voltage ramps from -60 to +100 mV; threshold was correlated with extracellular K+, so that at 10 mM K+, channels began to open at -30 mV. Evaluation of cell-cell communication using dual whole cell recordings from cell pairs revealed that activation of Panx1 current in one cell of the pair induced an inward current in the second cell after a latency of 10-20 s. This paracrine response was amplified by an ATPase inhibitor (ARL67156, 100 μM) and was blocked by the ATP-degrading enzyme apyrase (6.7 U/ml), by the P2 receptor antagonist suramin (50 μM) and by the Panx1 channel blocker carbenoxolone. These results provide additional evidence that ATP release through Panx1 channels can mediate nonsynaptic bidirectional intercellular communication. Furthermore, current potentiation by elevated K+ provides a mechanism for enhancement of ATP release under pathological conditions.
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