ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Regulation of postsynaptic Ca2+ influx in hippocampal CA1 pyramidal neurons via extracellular carbonic anhydrase.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Genomic predictors of remission to antidepressant treatment in geriatric depression using genome-wide expression analyses: a pilot study.International journal of geriatric psychiatry · 2016Trial
- pH regulating mechanisms of astrocytes: A critical component in physiology and disease of the brain.Cell calcium · 2024Review
- Carbonic anhydrase 4 disruption decreases synaptic and behavioral adaptations induced by cocaine withdrawal.Science advances · 2022Article
- Computational modeling predicts ephemeral acidic microdomains in the glutamatergic synaptic cleft.Biophysical journal · 2021Article
- Neuronal Glutamatergic Synaptic Clefts Alkalinize Rather Than Acidify during Neurotransmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- The role of glia in stress: polyamines and brain disorders.The Psychiatric clinics of North America · 2014Review
- Evidence from simultaneous intracellular- and surface-pH transients that carbonic anhydrase IV enhances CO2 fluxes across Xenopus oocyte plasma membranes.American journal of physiology. Cell physiology · 2014Article
- GPI-anchored carbonic anhydrase IV displays both intra- and extracellular activity in cRNA-injected oocytes and in mouse neurons.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- The transcriptomic response of mixed neuron-glial cell cultures to 1,25-dihydroxyvitamin d3 includes genes limiting the progression of neurodegenerative diseases.Journal of Alzheimer's disease : JAD · 2013Article
- NMDA receptor-dependent afterdepolarizations are curtailed by carbonic anhydrase 14: regulation of a short-term postsynaptic potentiation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Is there a path beyond BOLD? Molecular imaging of brain function.NeuroImage · 2012Review
- Inhibition of carbonic anhydrase reduces brain injury after intracerebral hemorrhage.Translational stroke research · 2012Article
- Calcium Signaling and Gliotransmission in Normal vs. Reactive Astrocytes.Frontiers in pharmacology · 2012Article
- Regulation of dendritic spine growth through activity-dependent recruitment of the brain-enriched Na⁺/H⁺ exchanger NHE5.Molecular biology of the cell · 2011Article
- Mobilization of calcium from intracellular stores facilitates somatodendritic dopamine release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Carbonic anhydrases CA4 and CA14 both enhance AE3-mediated Cl--HCO3- exchange in hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Endogenous alkaline transients boost postsynaptic NMDA receptor responses in hippocampal CA1 pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Synchronous neural activity causes rapid changes of extracellular pH (pH(e)) in the nervous system. In the CA1 region of the hippocampus, stimulation of the Schaffer collaterals elicits an alkaline pH(e) transient in stratum radiatum that is limited by extracellular carbonic anhydrase (ECA). When interstitial buffering is diminished by inhibition of ECA, the alkalosis is enhanced and NMDA receptor (NMDAR)-mediated postsynaptic currents can be augmented. Accordingly, the dendritic influx of Ca2+ elicited by synaptic excitation may be expected to increase if ECA activity were blocked. We tested this hypothesis in the CA1 stratum radiatum of hippocampal slices from juvenile rats, using extracellular, concentric pH- and Ca2+-selective microelectrodes with response times of a few milliseconds, as well as Fluo-5F imaging of intracellular Ca2+ transients. Brief stimulation of the Schaffer collaterals elicited an alkaline pH(e) transient, a transient decrease in free extracellular Ca2+ concentration ([Ca2+]e), and a corresponding transient rise in free intracellular Ca2+ concentration ([Ca2+]i). Inhibition of ECA with benzolamide caused a marked amplification and prolonged recovery of the pH(e) and [Ca2+]e responses, as well as the dendritic [Ca2+]i transients. The increase in amplitude caused by benzolamide did not occur in the presence of the NMDAR antagonist APV, but the decay of the responses was still prolonged. These results indicate that ECA can shape dendritic Ca2+ dynamics governed by NMDARs by virtue of its regulation of concomitant activity-dependent pH(e) shifts. The data also suggest that Ca2+ transients are influenced by additional mechanisms sensitive to shifts in pH(e).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.