FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1570295095> ?p ?o ?g. }

• W1570295095 endingPage "4386" @default.
• W1570295095 startingPage "4373" @default.
• W1570295095 abstract "Key points The hippocampal CA1 region is highly vulnerable to ischaemic stroke. Two forms of AMPA receptor (AMPAR) plasticity – an anoxic form of long‐term potentiation and a delayed increase in Ca 2+ ‐permeable (CP) AMPARs – contribute to this susceptibility by increasing excitotoxicity. In CA1, the acid‐sensing ion channel 1a (ASIC1a) is known to facilitate LTP and contribute to ischaemic acidotoxicity. We have examined the role of ASIC1a in AMPAR ischaemic plasticity in organotypic hippocampal slice cultures exposed to oxygen glucose deprivation (a model of ischaemic stroke), and in hippocampal pyramidal neuron cultures exposed to acidosis. We find that ASIC1a activation promotes both forms of AMPAR plasticity and that neuroprotection, by inhibiting ASIC1a, circumvents any further benefit of blocking CP‐AMPARs. Our observations establish a new interaction between acidotoxicity and excitotoxicity, and provide insight into the role of ASIC1a and CP‐AMPARs in neurodegeneration. Specifically, we propose that ASIC1a activation drives certain post‐ischaemic forms of CP‐AMPAR plasticity. Abstract The CA1 region of the hippocampus is particularly vulnerable to ischaemic damage. While NMDA receptors play a major role in excitotoxicity, it is thought to be exacerbated in this region by two forms of post‐ischaemic AMPA receptor (AMPAR) plasticity – namely, anoxic long‐term potentiation (a‐LTP), and a delayed increase in the prevalence of Ca 2+ ‐permeable GluA2‐lacking AMPARs (CP‐AMPARs). The acid‐sensing ion channel 1a (ASIC1a), which is expressed in CA1 pyramidal neurons, is also known to contribute to post‐ischaemic neuronal death and to physiologically induced LTP. This raises the question does ASIC1a activation drive the post‐ischaemic forms of AMPAR plasticity in CA1 pyramidal neurons? We have tested this by examining organotypic hippocampal slice cultures (OHSCs) exposed to oxygen glucose deprivation (OGD), and dissociated cultures of hippocampal pyramidal neurons (HPNs) exposed to low pH (acidosis). We find that both a‐LTP and the delayed increase in the prevalence of CP‐AMPARs are dependent on ASIC1a activation during ischaemia. Indeed, acidosis alone is sufficient to induce the increase in CP‐AMPARs. We also find that inhibition of ASIC1a channels circumvents any potential neuroprotective benefit arising from block of CP‐AMPARs. By demonstrating that ASIC1a activation contributes to post‐ischaemic AMPAR plasticity, our results identify a functional interaction between acidotoxicity and excitotoxicity in hippocampal CA1 cells, and provide insight into the role of ASIC1a and CP‐AMPARs as potential drug targets for neuroprotection. We thus propose that ASIC1a activation can drive certain forms of CP‐AMPAR plasticity, and that inhibiting ASIC1a affords neuroprotection." @default.
• W1570295095 created "2016-06-24" @default.
• W1570295095 creator A5048516955 @default.
• W1570295095 creator A5062263080 @default.
• W1570295095 creator A5069305015 @default.
• W1570295095 creator A5069396291 @default.
• W1570295095 creator A5071371736 @default.
• W1570295095 creator A5075057046 @default.
• W1570295095 creator A5079561004 @default.
• W1570295095 creator A5087503778 @default.
• W1570295095 date "2015-08-18" @default.
• W1570295095 modified "2023-10-03" @default.
• W1570295095 title "Acid-sensing ion channel 1a drives AMPA receptor plasticity following ischaemia and acidosis in hippocampal CA1 neurons" @default.
• W1570295095 cites W1576855071 @default.
• W1570295095 cites W1774281578 @default.
• W1570295095 cites W1986292636 @default.
• W1570295095 cites W1987556731 @default.
• W1570295095 cites W1987605877 @default.
• W1570295095 cites W1990269235 @default.
• W1570295095 cites W1993782794 @default.
• W1570295095 cites W1995966051 @default.
• W1570295095 cites W2000610579 @default.
• W1570295095 cites W2001646873 @default.
• W1570295095 cites W2002360249 @default.
• W1570295095 cites W2002974809 @default.
• W1570295095 cites W2003625042 @default.
• W1570295095 cites W2014696835 @default.
• W1570295095 cites W2015725815 @default.
• W1570295095 cites W2016550668 @default.
• W1570295095 cites W2019357760 @default.
• W1570295095 cites W2020622209 @default.
• W1570295095 cites W2020931572 @default.
• W1570295095 cites W2022036407 @default.
• W1570295095 cites W2031412579 @default.
• W1570295095 cites W2034879040 @default.
• W1570295095 cites W2036567510 @default.
• W1570295095 cites W2037341321 @default.
• W1570295095 cites W2055829165 @default.
• W1570295095 cites W2057823004 @default.
• W1570295095 cites W2058877455 @default.
• W1570295095 cites W2065171486 @default.
• W1570295095 cites W2070961029 @default.
• W1570295095 cites W2073585436 @default.
• W1570295095 cites W2078799316 @default.
• W1570295095 cites W2079054696 @default.
• W1570295095 cites W2080203024 @default.
• W1570295095 cites W2085805107 @default.
• W1570295095 cites W2086688096 @default.
• W1570295095 cites W2087706333 @default.
• W1570295095 cites W2087807100 @default.
• W1570295095 cites W2088912287 @default.
• W1570295095 cites W2089817334 @default.
• W1570295095 cites W2112128826 @default.
• W1570295095 cites W2119067306 @default.
• W1570295095 cites W2126443053 @default.
• W1570295095 cites W2128104071 @default.
• W1570295095 cites W2130630814 @default.
• W1570295095 cites W2137970237 @default.
• W1570295095 cites W2161056273 @default.
• W1570295095 cites W4245792346 @default.
• W1570295095 doi "https://doi.org/10.1113/jp270701" @default.
• W1570295095 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4594240" @default.
• W1570295095 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26174503" @default.
• W1570295095 hasPublicationYear "2015" @default.
• W1570295095 type Work @default.
• W1570295095 sameAs 1570295095 @default.
• W1570295095 citedByCount "31" @default.
• W1570295095 countsByYear W15702950952016 @default.
• W1570295095 countsByYear W15702950952017 @default.
• W1570295095 countsByYear W15702950952018 @default.
• W1570295095 countsByYear W15702950952019 @default.
• W1570295095 countsByYear W15702950952020 @default.
• W1570295095 countsByYear W15702950952021 @default.
• W1570295095 countsByYear W15702950952022 @default.
• W1570295095 countsByYear W15702950952023 @default.
• W1570295095 crossrefType "journal-article" @default.
• W1570295095 hasAuthorship W1570295095A5048516955 @default.
• W1570295095 hasAuthorship W1570295095A5062263080 @default.
• W1570295095 hasAuthorship W1570295095A5069305015 @default.
• W1570295095 hasAuthorship W1570295095A5069396291 @default.
• W1570295095 hasAuthorship W1570295095A5071371736 @default.
• W1570295095 hasAuthorship W1570295095A5075057046 @default.
• W1570295095 hasAuthorship W1570295095A5079561004 @default.
• W1570295095 hasAuthorship W1570295095A5087503778 @default.
• W1570295095 hasBestOaLocation W15702950951 @default.
• W1570295095 hasConcept C126322002 @default.
• W1570295095 hasConcept C148762608 @default.
• W1570295095 hasConcept C160268369 @default.
• W1570295095 hasConcept C169760540 @default.
• W1570295095 hasConcept C170493617 @default.
• W1570295095 hasConcept C185592680 @default.
• W1570295095 hasConcept C25274449 @default.
• W1570295095 hasConcept C25498285 @default.
• W1570295095 hasConcept C2781012912 @default.
• W1570295095 hasConcept C61174792 @default.
• W1570295095 hasConcept C71924100 @default.
• W1570295095 hasConcept C86803240 @default.
• W1570295095 hasConcept C98229152 @default.

• next