ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Compensatory enhancement of intrinsic spiking upon NKCC1 disruption in neonatal hippocampus.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 76 citations in OpenAlex.
- Bumetanide for autism: more eye contact, less amygdala activation.Scientific reports · 2018Trial
- Expression patterns of NKCC1 in neurons and non-neuronal cells during cortico-hippocampal development.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- How Staying Negative Is Good for the (Adult) Brain: Maintaining Chloride Homeostasis and the GABA-Shift in Neurological Disorders.Frontiers in molecular neuroscience · 2022Review
- Unique Actions of GABA Arising from Cytoplasmic Chloride Microdomains.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- A limited role of NKCC1 in telencephalic glutamatergic neurons for developing hippocampal network dynamics and behavior.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Gabaergic Interneurons in Early Brain Development: Conducting and Orchestrated by Cortical Network Activity.Frontiers in molecular neuroscience · 2021Article
- NKCC1, an Elusive Molecular Target in Brain Development: Making Sense of the Existing Data.Cells · 2020Review
- NKCC-1 mediated ClScientific reports · 2020Article
- Staurosporine and NEM mainly impair WNK-SPAK/OSR1 mediated phosphorylation of KCC2 and NKCC1.PloS one · 2020Article
- Spontaneous Ultraslow NaCells · 2019Article
- Understanding intellectual disability and autism spectrum disorders from common mouse models: synapses to behaviour.Open biology · 2019Review
- KCC2-Mediated ClCell reports · 2019Article
- Chloride Dysregulation, Seizures, and Cerebral Edema: A Relationship with Therapeutic Potential.Trends in neurosciences · 2017Review
- Early Correlated Network Activity in the Hippocampus: Its Putative Role in Shaping Neuronal Circuits.Frontiers in cellular neuroscience · 2017Review
- Interneurons Differentially Contribute to Spontaneous Network Activity in the Developing Hippocampus Dependent on Their Embryonic Lineage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Acute and chronic efficacy of bumetanide in an in vitro model of posttraumatic epileptogenesis.CNS neuroscience & therapeutics · 2015Article
- Chloride Accumulators NKCC1 and AE2 in Mouse GnRH Neurons: Implications for GABAA Mediated Excitation.PloS one · 2015Article
- Prenatal Hypoxia-Ischemia Induces Abnormalities in CA3 Microstructure, Potassium Chloride Co-Transporter 2 Expression and Inhibitory Tone.Frontiers in cellular neuroscience · 2015Article
- Novel determinants of the neuronal Cl(-) concentration.The Journal of physiology · 2014Review
- Cation-chloride cotransporters in neuronal development, plasticity and disease.Nature reviews. Neuroscience · 2014Review
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7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Depolarizing and excitatory GABA actions are thought to be important in cortical development. We show here that GABA has no excitatory action on CA3 pyramidal neurons in hippocampal slices from neonatal NKCC1(-/-) mice that lack the Na-K-2Cl cotransporter isoform 1. Strikingly, NKCC1(-/-) slices generated endogenous network events similar to giant depolarizing potentials (GDPs), but, unlike in wild-type slices, the GDPs were not facilitated by the GABA(A) agonist isoguvacine or blocked by the NKCC1 inhibitor bumetanide. The developmental upregulation of the K-Cl cotransporter 2 (KCC2) was unperturbed, whereas the pharmacologically isolated glutamatergic network activity and the intrinsic excitability of CA3 pyramidal neurons were enhanced in the NKCC1(-/-) hippocampus. Hence, developmental expression of KCC2, unsilencing of AMPA-type synapses, and early network events can take place in the absence of excitatory GABAergic signaling in the neonatal hippocampus. Furthermore, we show that genetic as well as pharmacologically induced loss of NKCC1-dependent excitatory actions of GABA results in a dramatic compensatory increase in the intrinsic excitability of glutamatergic neurons, pointing to powerful homeostatic regulation of neuronal activity in the developing hippocampal circuitry.
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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.