ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Contribution of the Na-K-Cl cotransporter on GABA(A) receptor-mediated presynaptic depolarization in excitatory nerve terminals.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. 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, 98 citations in OpenAlex.
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- Activity-Dependent Ectopic Spiking in Parvalbumin-Expressing Interneurons of the Neocortex.eNeuro · 2024Article
- NKCC1 and KCC2 Chloride Transporters Have Different Membrane Dynamics on the Surface of Hippocampal Neurons.Cells · 2023Article
- Expression patterns of NKCC1 in neurons and non-neuronal cells during cortico-hippocampal development.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- NKCC1, an Elusive Molecular Target in Brain Development: Making Sense of the Existing Data.Cells · 2020Review
- Calcium-engaged Mechanisms of Nongenomic Action of Neurosteroids.Current neuropharmacology · 2017Review
- A novel GABA-mediated corticotropin-releasing hormone secretory mechanism in the median eminence.Science advances · 2016Article
- Modulation of spontaneous intracellular Ca²⁺ fluctuations and spontaneous cholinergic transmission in rat chromaffin cells in situ by endogenous GABA acting on GABAA receptors.Pflugers Archiv : European journal of physiology · 2016Article
- Presynaptic gating of excitation in the dorsal raphe nucleus by GABA.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Presynaptic glycine receptors increase GABAergic neurotransmission in rat periaqueductal gray neurons.Neural plasticity · 2013Article
- GABAergic synaptic transmission triggers action potentials in thalamic reticular nucleus neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Ionotropic receptors at hippocampal mossy fibers: roles in axonal excitability, synaptic transmission, and plasticity.Frontiers in neural circuits · 2012Article
- Modulation of presynaptic GABA(A) receptors by endogenous neurosteroids.British journal of pharmacology · 2011Article
- A conserved asparagine residue in transmembrane segment 1 (TM1) of serotonin transporter dictates chloride-coupled neurotransmitter transport.The Journal of biological chemistry · 2011Article
- Axonal GABAA receptors increase cerebellar granule cell excitability and synaptic activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Presynaptic glycine receptors influence plasma membrane potential and glutamate release.Neurochemical research · 2010Article
- Retinal input to efferent target amacrine cells in the avian retina.Visual neuroscience · 2010Article
- Propofol facilitates glutamatergic transmission to neurons of the ventrolateral preoptic nucleus.Anesthesiology · 2009Article
- GABA(A) autoreceptors enhance GABA release from human neocortex: towards a mechanism for high-frequency stimulation (HFS) in brain?Naunyn-Schmiedeberg's archives of pharmacology · 2009Article
Corrections and comments
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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
GABA(A) receptor-mediated responses manifest as either hyperpolarization or depolarization according to the intracellular Cl(-) concentration ([Cl(-)](i)). Here, we report a novel functional interaction between the Na-K-Cl cotransporter (NKCC) and GABA(A) receptor actions on glutamatergic presynaptic nerve terminals projecting to ventromedial hypothalamic (VMH) neurons. The activation of presynaptic GABA(A) receptors depolarizes the presynaptic nerve terminals and facilitates spontaneous glutamate release by activating TTX-sensitive Na(+) channels and high-threshold Ca(2+) channels. This depolarizing action of GABA was caused by an outwardly directed Cl(-) driving force for GABA(A) receptors; that is, the [Cl(-)](i) of glutamatergic nerve terminals was higher than that predicted for a passive distribution. The higher [Cl(-)](i) was generated by bumetanide-sensitive NKCCs and was responsible for the GABA-induced presynaptic depolarization. Thus, GABA(A) receptor-mediated modulation of spontaneous glutamatergic transmission may contribute to the development and regulation of VMH function as well as to the excitability of VMH neurons themselves.
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11487619PMC6763144W1563946002What 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.