ArticleProceedings of the National Academy of Sciences of the United States of America2008
Acid-sensing ion channels interact with and inhibit BK K+ channels.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- Acid-sensing ion channels and their role in controlling pain in the post-operative stage.International journal of physiology, pathophysiology and pharmacology · 2026Review
- Review
- Cell Settling, Migration, and Stochastic Cancer Gene Expression Suggest Potassium Membrane Flux May Initiate pH Reversal.Biomolecules · 2025Article
- The diverse functions of the DEG/ENaC family: linking genetic and physiological insights.The Journal of physiology · 2023Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Acid-sensing ion channel 1a activates IKCa/SKCa channels and contributes to endothelium-dependent dilation.The Journal of general physiology · 2023Article
- Acid sensing ion channel 2: A new potential player in the pathophysiology of multiple sclerosis.The European journal of neuroscience · 2019Article
- Human ASIC1a mediates stronger acid-induced responses as compared with mouse ASIC1a.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Cellular Localization of Acid-Sensing Ion Channel 1 in Rat Nucleus Tractus Solitarii.Cellular and molecular neurobiology · 2018Article
- The synaptic action of Degenerin/Epithelial sodium channels.Channels (Austin, Tex.) · 2018Review
- Glucose Deficiency Elevates Acid-Sensing Ion Channel 2a Expression and Increases Seizure Susceptibility in Temporal Lobe Epilepsy.Scientific reports · 2017Article
- TheThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- The function and regulation of acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC): IUPHAR Review 19.British journal of pharmacology · 2016Review
- Two di-leucine motifs regulate trafficking and function of mouse ASIC2a.Molecular brain · 2016Article
- Acid-sensing ion channel 1a contributes to the effect of extracellular acidosis on NLRP1 inflammasome activation in cortical neurons.Journal of neuroinflammation · 2015Article
- ASICs and cardiovascular homeostasis.Neuropharmacology · 2015Review
- Effect of activation of the Ca(2+)-permeable acid-sensing ion channel 1a on focal cerebral ischemia in diabetic rats.International journal of clinical and experimental pathology · 2015Article
- Acid-sensing ion channels 1a (ASIC1a) inhibit neuromuscular transmission in female mice.American journal of physiology. Cell physiology · 2014Article
- Responses of glomus cells to hypoxia and acidosis are uncoupled, reciprocal and linked to ASIC3 expression: selectivity of chemosensory transduction.The Journal of physiology · 2013Article
- Acid sensing ion channels regulate neuronal excitability by inhibiting BK potassium channels.Biochemical and biophysical research communications · 2012Article
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Acid-sensing ion channels (ASICs) are neuronal non-voltage-gated cation channels that are activated when extracellular pH falls. They contribute to sensory function and nociception in the peripheral nervous system, and in the brain they contribute to synaptic plasticity and fear responses. Some of the physiologic consequences of disrupting ASIC genes in mice suggested that ASIC channels might modulate neuronal function by mechanisms in addition to their H(+)-evoked opening. Within ASIC channel's large extracellular domain, we identified sequence resembling that in scorpion toxins that inhibit K(+) channels. Therefore, we tested the hypothesis that ASIC channels might inhibit K(+) channel function by coexpressing ASIC1a and the high-conductance Ca(2+)- and voltage-activated K(+) (BK) channel. We found that ASIC1a associated with BK channels and inhibited their current. Reducing extracellular pH disrupted the association and relieved the inhibition. BK channels, in turn, altered the kinetics of ASIC1a current. In addition to BK, ASIC1a inhibited voltage-gated Kv1.3 channels. Other ASIC channels also inhibited BK, although acidosis-dependent relief of inhibition varied. These results reveal a mechanism of ion channel interaction and reciprocal regulation. Finding that a reduced pH activated ASIC1a and relieved BK inhibition suggests that extracellular protons may enhance the activity of channels with opposing effects on membrane voltage. The wide and varied expression patterns of ASICs, BK, and related K(+) channels suggest broad opportunities for this signaling system to alter neuronal function.
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