ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1996
Excitatory actions of GABA after neuronal trauma.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
81 citing papers in PubMed, 233 citations in OpenAlex.
- WNK-SPAK/OSR1 signaling pathway facilitates ictal activity via reduced neuronal chloride extrusion rate.bioRxiv : the preprint server for biology · 2026Article
- Alterations in the Components of the GABA-Glutamate System During ZIKV Infection: A Neuroscience Approach.International journal of molecular sciences · 2026Article
- Electroactive biomaterials modulating ion channels in nervous system regeneration.Regenerative biomaterials · 2026Review
- The Role of Nanotechnology in Understanding the Pathophysiology of Traumatic Brain Injury.Central nervous system agents in medicinal chemistry · 2025Review
- Oxytocin Exhibits Neuroprotective Effects on Hippocampal Cultures under Severe Oxygen-Glucose Deprivation Conditions.Current issues in molecular biology · 2024Article
- Depolarization of mouse DRG neurons by GABA does not translate into acute pain or hyperalgesia in healthy human volunteers.PloS one · 2024Article
- Pluripotential GluN1 (NMDA NR1): Functional Significance in Cellular Nuclei in Pain/Nociception.International journal of molecular sciences · 2023Review
- Are GABAergic drugs beneficial in providing neuroprotection after traumatic brain injuries? A comprehensive literature review of preclinical studies.Frontiers in neurology · 2023Review
- Non-Targeted Metabolomics Approach Revealed Significant Changes in Metabolic Pathways in Patients with Chronic Traumatic Encephalopathy.Biomedicines · 2022Article
- Non-monotonic effects of GABAergic synaptic inputs on neuronal firing.PLoS computational biology · 2022Article
- Zolpidem Profoundly Augments Spared Tonic GABAFrontiers in systems neuroscience · 2022Article
- Biophysical Modeling Suggests Optimal Drug Combinations for Improving the Efficacy of GABA Agonists after Traumatic Brain Injuries.Journal of neurotrauma · 2019Article
- Three-dimensional (3D) brain microphysiological system for organophosphates and neurochemical agent toxicity screening.PloS one · 2019Article
- Alterations in the Timing of Huperzine A Cerebral Pharmacodynamics in the Acute Traumatic Brain Injury Setting.Journal of neurotrauma · 2018Article
- Chloride Dysregulation, Seizures, and Cerebral Edema: A Relationship with Therapeutic Potential.Trends in neurosciences · 2017Review
- Chronic Unpredictable Mild Stress Induces Loss of GABA Inhibition in Corticotrophin-Releasing Hormone-Expressing Neurons through NKCC1 Upregulation.Neuroendocrinology · 2017Article
- Circadian variability of the initial Glasgow Coma Scale score in traumatic brain injury patients.Neurobiology of sleep and circadian rhythms · 2017Article
- An Optogenetic Approach for Investigation of Excitatory and Inhibitory Network GABA Actions in Mice Expressing Channelrhodopsin-2 in GABAergic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Neuroblast Distribution after Cortical Impact Is Influenced by White Matter Injury in the Immature Gyrencephalic Brain.Frontiers in neuroscience · 2016Article
- Developmental Decrease of Neuronal Chloride Concentration Is Independent of Trauma in Thalamocortical Brain Slices.PloS one · 2016Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
GABA is the dominant inhibitory neurotransmitter in the CNS. By opening Cl- channels, GABA generally hyperpolarizes the membrane potential, decreases neuronal activity, and reduces intracellular Ca2+ of mature neurons. In the present experiment, we show that after neuronal trauma, GABA, both synaptically released and exogenously applied, exerted a novel and opposite effect, depolarizing neurons and increasing intracellular Ca2+. Different types of trauma that were effective included neurite transection, replating, osmotic imbalance, and excess heat. The depolarizing actions of GABA after trauma increased Ca2+ levels up to fourfold in some neurons, occurred in more than half of the severely injured neurons, and was long lasting (>1 week). The mechanism for the reversed action of GABA appears to be a depolarized Cl- reversal potential that results in outward rather than inward movement of Cl-, as revealed by gramicidin-perforated whole-cell patch-clamp recording. The consequent depolarization and resultant activation of the nimodipine sensitive L- and conotoxin-sensitive N-type voltage-activated Ca2+ channel allows extracellular Ca2+ to enter the neuron. The long-lasting capacity to raise Ca2+ may give GABA a greater role during recovery from trauma in modulating gene expression, and directing and enhancing outgrowth of regenerating neurites. On the negative side, by its depolarizing actions, GABA could increase neuronal damage by raising cytosolic Ca2+ levels in injured cells. Furthermore, the excitatory actions of GABA after neuronal injury may contribute to maladaptive signal transmission in affected GABAergic brain circuits.
Indexed as
Identifiers
8753889PMC6578987W2119350525What 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.