ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Endogenous alkaline transients boost postsynaptic NMDA receptor responses in hippocampal CA1 pyramidal neurons.
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 27 papers.
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Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
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- Postsynaptic Calcium Extrusion at the Mouse Neuromuscular Junction Alkalinizes the Synaptic Cleft.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- GluD receptors are functional ion channels.Biophysical journal · 2023Review
- Computational modeling predicts ephemeral acidic microdomains in the glutamatergic synaptic cleft.Biophysical journal · 2021Article
- A GlutamateThe Journal of pharmacology and experimental therapeutics · 2021Article
- Neurodegenerative Disease: What Potential Therapeutic Role of Acid-Sensing Ion Channels?Frontiers in cellular neuroscience · 2021Review
- Neuronal Glutamatergic Synaptic Clefts Alkalinize Rather Than Acidify during Neurotransmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Developmental maturation of activity-induced KThe Journal of physiology · 2019Article
- Rescue of hyperexcitability in hippocampal CA1 neurons from Mecp2 (-/y) mouse through surface potential neutralization.PloS one · 2018Article
- Mouse Slc4a11 expressed in Xenopus oocytes is an ideally selective H+/OH- conductance pathway that is stimulated by rises in intracellular and extracellular pH.American journal of physiology. Cell physiology · 2016Article
- Autocrine boost of NMDAR current in hippocampal CA1 pyramidal neurons by a PMCA-dependent, perisynaptic, extracellular pH shift.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Intracellular pH regulation by acid-base transporters in mammalian neurons.Frontiers in physiology · 2014Review
- 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
- pH-dependent inhibition of native GABA(A) receptors by HEPES.British journal of pharmacology · 2012Article
- The sodium-driven chloride/bicarbonate exchanger in presynaptic terminals.The Journal of comparative neurology · 2012Article
- A steroid modulatory domain in NR2A collaborates with NR1 exon-5 to control NMDAR modulation by pregnenolone sulfate and protons.Journal of neurochemistry · 2011Article
- Regulation of dendritic spine growth through activity-dependent recruitment of the brain-enriched Na⁺/H⁺ exchanger NHE5.Molecular biology of the cell · 2011Article
- Neurobiology of panic and pH chemosensation in the brain.Dialogues in clinical neuroscience · 2011Review
- Synaptic acidification enhances GABAA signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Excessive Na+/H+ exchange in disruption of dendritic Na+ and Ca2+ homeostasis and mitochondrial dysfunction following in vitro ischemia.The Journal of biological chemistry · 2010Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In hippocampus, activation of the Schaffer collaterals generates an extracellular alkaline transient both in vitro and in vivo. This pH change may provide relief of the H+ block of NMDA receptors (NMDARs) and thereby increase excitability. To test this hypothesis, we augmented extracellular buffering in mouse hippocampal slices by adding 2 microM bovine type II carbonic anhydrase to the superfusate. With addition of enzyme, the alkaline transient elicited by a 10 pulse, 100 Hz stimulus train was reduced by 33%. At a holding potential (V(H)) of -30 mV, the enzyme decreased the half-time of decay and charge transfer of EPSCs by 32 and 39%, respectively, but had no effect at a V(H) of -80 mV. In current clamp, a 10 pulse, 100 Hz stimulus train gave rise to an NMDAR-dependent afterdepolarization (ADP). Exogenous enzyme curtailed the ADP half-width and voltage integral by 20 and 25%, respectively. Similar reduction of the ADP was noted with a brief 12 Hz stimulus train. The effect persisted in the presence of GABAergic antagonists or the L-type Ca2+ channel blocker methoxyverapamil hydrochloride but was absent in the presence of the carbonic anhydrase inhibitor benzolamide or when the exogenous enzyme was heat inactivated. The effects of the enzyme in voltage and current clamp were noted in 0 Mg2+ media but were abolished when (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine maleate was included in the patch pipette. These results provide strong evidence that endogenous alkaline transients are sufficiently large in the vicinity of the synapse to augment NMDAR responses.
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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.