ArticleJournal of neurophysiology2009
NKCC1 and AE3 appear to accumulate chloride in embryonic motoneurons.
Article in Journal of neurophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 78 citations in OpenAlex.
- Chloride Homeostasis in Neuronal Disorders: Bridging Measurement to Therapy.Life (Basel, Switzerland) · 2025Review
- Massive Activation of GABABiomolecules · 2025Review
- Chloride Modulates Central pH Sensitivity and Plasticity of Brainstem Breathing-Related Biorhythms in Zebra Finch Embryos.Developmental psychobiology · 2024Article
- Evidence for Two Subpopulations of Cerebrospinal Fluid-Contacting Neurons with Opposite GABAergic Signaling in Adult Mouse Spinal Cord.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Glycine neurotransmission: Its role in development.Frontiers in neuroscience · 2022Review
- Homeostatic Regulation of Motoneuron Properties in Development.Advances in neurobiology · 2022Review
- Chloride Homeostasis in Developing Motoneurons.Advances in neurobiology · 2022Article
- Intricacies of GABAInternational journal of molecular sciences · 2021Review
- When Are Depolarizing GABAergic Responses Excitatory?Frontiers in molecular neuroscience · 2021Review
- Coincident glutamatergic depolarizations enhance GABAA receptor-dependent Cl- influx in mature and suppress Cl- efflux in immature neurons.PLoS computational biology · 2021Article
- NKCC-1 mediated ClScientific reports · 2020Article
- Interactions between Membrane Resistance, GABA-A Receptor Properties, Bicarbonate Dynamics and ClInternational journal of molecular sciences · 2019Article
- Regulation of synaptic scaling by action potential-independent miniature neurotransmission.Journal of neuroscience research · 2018Review
- Elevated intracellular NaJournal of neurochemistry · 2017Article
- Activity-dependent plasticity in the isolated embryonic avian brainstem following manipulations of rhythmic spontaneous neural activity.Respiratory physiology & neurobiology · 2016Article
- Glycinergic Neurotransmission: A Potent Regulator of Embryonic Motor Neuron Dendritic Morphology and Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Depolarizing GABA and developmental epilepsies.CNS neuroscience & therapeutics · 2015Review
- Chloride Accumulators NKCC1 and AE2 in Mouse GnRH Neurons: Implications for GABAA Mediated Excitation.PloS one · 2015Article
- GABAA receptor-mediated tonic depolarization in developing neural circuits.Molecular neurobiology · 2014Review
- Circadian modulation of the Cl(-) equilibrium potential in the rat suprachiasmatic nuclei.BioMed research international · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
During early development, gamma-aminobutyric acid (GABA) depolarizes and excites neurons, contrary to its typical function in the mature nervous system. As a result, developing networks are hyperexcitable and experience a spontaneous network activity that is important for several aspects of development. GABA is depolarizing because chloride is accumulated beyond its passive distribution in these developing cells. Identifying all of the transporters that accumulate chloride in immature neurons has been elusive and it is unknown whether chloride levels are different at synaptic and extrasynaptic locations. We have therefore assessed intracellular chloride levels specifically at synaptic locations in embryonic motoneurons by measuring the GABAergic reversal potential (EGABA) for GABAA miniature postsynaptic currents. When whole cell patch solutions contained 17-52 mM chloride, we found that synaptic EGABA was around -30 mV. Because of the low HCO3- permeability of the GABAA receptor, this value of EGABA corresponds to approximately 50 mM intracellular chloride. It is likely that synaptic chloride is maintained at levels higher than the patch solution by chloride accumulators. We show that the Na+-K+-2Cl- cotransporter, NKCC1, is clearly involved in the accumulation of chloride in motoneurons because blocking this transporter hyperpolarized EGABA and reduced nerve potentials evoked by local application of a GABAA agonist. However, chloride accumulation following NKCC1 block was still clearly present. We find physiological evidence of chloride accumulation that is dependent on HCO3- and sensitive to an anion exchanger blocker. These results suggest that the anion exchanger, AE3, is also likely to contribute to chloride accumulation in embryonic motoneurons.
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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.