ArticleThe Journal of physiology2003
Hyperpolarizing inhibition develops without trophic support by GABA in cultured rat midbrain neurons.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 74 citations in OpenAlex.
- The role of immune regulation in peripheral nerve regeneration: functions of inflammatory cells and cytokines.Frontiers in pharmacology · 2026Review
- Gabaergic Interneurons in Early Brain Development: Conducting and Orchestrated by Cortical Network Activity.Frontiers in molecular neuroscience · 2021Article
- When Are Depolarizing GABAergic Responses Excitatory?Frontiers in molecular neuroscience · 2021Review
- Coincident Activation of Glutamate Receptors Enhances GABAFrontiers in cellular neuroscience · 2019Article
- KCC2 knockdown impairs glycinergic synapse maturation in cultured spinal cord neurons.Histochemistry and cell biology · 2016Article
- Hyperpolarization-independent maturation and refinement of GABA/glycinergic connections in the auditory brain stem.Journal of neurophysiology · 2016Article
- Etiology of distinct membrane excitability in pre- and posthearing auditory neurons relies on activity of Cl- channel TMEM16A.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Cation-chloride cotransporters in neuronal development, plasticity and disease.Nature reviews. Neuroscience · 2014Review
- Spontaneous Network Activity and Synaptic Development.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2014Review
- Current view on the functional regulation of the neuronal K(+)-Cl(-) cotransporter KCC2.Frontiers in cellular neuroscience · 2014Review
- An unexpected role of neuroligin-2 in regulating KCC2 and GABA functional switch.Molecular brain · 2013Article
- Effects of third trimester-equivalent ethanol exposure on Cl(-) co-transporter expression, network activity, and GABAergic transmission in the CA3 hippocampal region of neonatal rats.Alcohol (Fayetteville, N.Y.) · 2012Article
- Sphingosine-1-phosphate links glycosphingolipid metabolism to neurodegeneration via a calpain-mediated mechanism.Cell death and differentiation · 2011Article
- Development of cortical GABAergic innervation.Frontiers in cellular neuroscience · 2011Article
- Non-cell-autonomous factor induces the transition from excitatory to inhibitory GABA signaling in retina independent of activity.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Contribution of GABAergic interneurons to the development of spontaneous activity patterns in cultured neocortical networks.Frontiers in cellular neuroscience · 2010Article
- Compensatory enhancement of intrinsic spiking upon NKCC1 disruption in neonatal hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Article
- NKCC1-dependent GABAergic excitation drives synaptic network maturation during early hippocampal development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Lysosulfatide regulates the motility of a neural precursor cell line via calcium-mediated process collapse.Neurochemical research · 2009Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During a limited period of early neuronal development, GABA is depolarizing and elevates [Ca2+]i, which mediates the trophic action of GABA in neuronal maturation. We tested the attractive hypothesis that GABA itself promotes the developmental change of its response from depolarizing to hyperpolarizing (Ganguly et al. 2001). In cultured midbrain neurons we found that the GABA response changed from depolarizing to hyperpolarizing, although GABAA receptors had been blocked throughout development. In immature neurons prolonged exposure of the cells to nanomolar concentrations of GABA or brief repetitive applications of GABA strongly diminished the elevation of [Ca+]i by GABA. As revealed by gramicidin perforated-patch recording, reduced [Ca2+]i responses were due to a diminished driving force for Cl-. This suggests that immature neurons do not have an efficient inward transport that can compensate the loss of cytosolic Cl-resulting from sustained GABAA receptor activation by ambient GABA. Transient increases in external K+, which can induce voltage-dependent Cl- entry, restored GABA-induced [Ca2+]i elevations. In mature neurons, GABA reduced [Ca2+]i provided that background [Ca2+]i was elevated by the application of an L-type Ca2+ channel agonist. This was probably due to a hyperpolarization of the membrane by Cl- currents. K(+)-Cl- cotransport maintained the gradient for hyperpolarizing Cl-currents. We conclude that in immature midbrain neurons an inward Cl- transport is not effective although the GABA response is depolarizing. Further, GABA itself is not required for the developmental switch of GABAergic responses from depolarizing to hyperpolarizing in cultured midbrain neurons.
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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.