ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Role of bicarbonate and chloride in GABA- and glycine-induced depolarization and [Ca2+]i rise in fetal rat motoneurons in situ.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 47 citations in OpenAlex.
- Presynaptic chloride-dependent regulation of spontaneous glutamate release in the rat medial preoptic nucleus.Frontiers in cellular neuroscience · 2026Article
- Massive Activation of GABABiomolecules · 2025Review
- KCC2 knockdown impairs glycinergic synapse maturation in cultured spinal cord neurons.Histochemistry and cell biology · 2016Article
- Anion transport and GABA signaling.Frontiers in cellular neuroscience · 2013Review
- NKCC1 and AE3 appear to accumulate chloride in embryonic motoneurons.Journal of neurophysiology · 2009Article
- Living or dying in three quarter time: neonatal orchestration of hippocampal cell death pathways by androgens and excitatory GABA.Experimental neurology · 2008Review
- Spontaneous rhythmic activity in early chick spinal cord influences distinct motor axon pathfinding decisions.Brain research reviews · 2008Review
- Dual personality of GABA/glycine-mediated depolarizations in immature spinal cord.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Increasing the frequency of spontaneous rhythmic activity disrupts pool-specific axon fasciculation and pathfinding of embryonic spinal motoneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Differential maturation of GABA action and anion reversal potential in spinal lamina I neurons: impact of chloride extrusion capacity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Glycinergic and GABAergic synaptic activity differentially regulate motoneuron survival and skeletal muscle innervation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Characterization of the circuits that generate spontaneous episodes of activity in the early embryonic mouse spinal cord.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Basis of changes in left-right coordination of rhythmic motor activity during development in the rat spinal cord.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- GABA-mediated Ca2+ signalling in developing rat cerebellar Purkinje neurones.The Journal of physiology · 2001Article
- A critical role of the strychnine-sensitive glycinergic system in spontaneous retinal waves of the developing rabbit.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca(2+) imaging and (perforated) patch recording were used to analyze the mechanism of GABA- and glycine-induced depolarizations in lumbar motoneurons of spinal cord slices from fetal rats. In fura-2 ester-loaded cells, the agonist-induced depolarizations increased [Ca(2+)](i) by up to 100 nm. The GABA- and glycine-evoked [Ca(2+)](i) transients were suppressed by bicuculline and strychnine, respectively. Their magnitude decreased by approximately 50% between embryonic days 15.5 and 19.5. The [Ca(2+)](i) increases were abolished by Ca(2+)-free superfusate and attenuated by approximately 65% by nifedipine, showing that the responses were mediated by voltage-activated Ca(2+) channels. The [Ca(2+)](i) rises were potentiated by >300% immediately after removal of Cl(-) from the superfusate but recovered to values of 50-200% of control during repeated agonist administration in Cl(-)-free saline. Bumetanide gradually suppressed the [Ca(2+)](i) increases by >75%. Subsequent removal of Cl(-) reconstituted the responses and increased, upon repeated agonist application, the peak [Ca(2+)](i) rises to values above control. Removal of HCO(3)(-) from the Cl(-)-free (bumetanide-containing) superfusate reversibly abolished both the agonist-induced [Ca(2+)](i) rises and depolarizations that were reestablished by formate anions. In Cl(-)-containing superfusate, removal of HCO(3)(-) decreased both the peak and duration of the agonist-evoked membrane depolarization and [Ca(2+)](i) response. Our findings show that HCO(3)(-) efflux has a major contribution to depolarizations mediated by GABA(A) and glycine receptor-coupled anion channels in prenatal neurons. We hypothesize that the HCO(3)(-)-dependent depolarizing component, which is likely to produce an intracellular acidosis, might play an important role during the early postnatal period when the Cl(-)-dependent component gradually shifts to hyperpolarization.
Indexed as
Identifiers
11050110PMC6772719W1695024632What OpenQuestion holds
Registered trials
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.