ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Aberrant chloride transport contributes to anoxic/ischemic white matter injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 47 citations in OpenAlex.
- Physiology of Oligodendroglia.Advances in neurobiology · 2025Review
- Glutamate-releasing BEST1 channel is a new target for neuroprotection against ischemic stroke with wide time window.Acta pharmaceutica Sinica. B · 2023Article
- Neuron to Oligodendrocyte Precursor Cell Synapses: Protagonists in Oligodendrocyte Development and Myelination, and Targets for Therapeutics.Frontiers in neuroscience · 2021Review
- Preserving Mitochondrial Structure and Motility Promotes Recovery of White Matter After Ischemia.Neuromolecular medicine · 2019Article
- A Review ofFrontiers in neuroscience · 2019Review
- Changes in gap junction expression and function following ischemic injury of spinal cord white matter.Journal of neurophysiology · 2014Article
- Expression of the γ2-subunit distinguishes synaptic and extrasynaptic GABA(A) receptors in NG2 cells of the hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Ionic transporter activity in astrocytes, microglia, and oligodendrocytes during brain ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013Review
- Highly conductive carbon nanotube matrix accelerates developmental chloride extrusion in central nervous system neurons by increased expression of chloride transporter KCC2.Small (Weinheim an der Bergstrasse, Germany) · 2013Article
- Research on ionic homeostatic equilibrium may change our view about epilepsy.Clinics (Sao Paulo, Brazil) · 2013Article
- Glial K⁺ clearance and cell swelling: key roles for cotransporters and pumps.Neurochemical research · 2012Review
- Creatine pretreatment protects cortical axons from energy depletion in vitro.Neurobiology of disease · 2012Article
- Aquaporins in spinal cord injury: the janus face of aquaporin 4.Neuroscience · 2010Review
- Loss of cation-chloride cotransporter expression in preterm infants with white matter lesions: implications for the pathogenesis of epilepsy.Journal of neuropathology and experimental neurology · 2010Article
- Neuroanatomic relationships between the GABAergic and serotonergic systems in the developing human medulla.Autonomic neuroscience : basic & clinical · 2010Article
- Effects of the noradrenergic system in rat white matter exposed to oxygen-glucose deprivation in vitro.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Complex interplay between glutamate receptors and intracellular Ca2+ stores during ischaemia in rat spinal cord white matter.The Journal of physiology · 2006Article
- Na+-dependent sources of intra-axonal Ca2+ release in rat optic nerve during in vitro chemical ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Regulation of K-Cl cotransport: from function to genes.The Journal of membrane biology · 2004Review
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Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Rundown of ionic gradients is a central feature of white matter anoxic injury; however, little is known about the contribution of anions such as Cl-. We used the in vitro rat optic nerve to study the role of aberrant Cl- transport in anoxia/ischemia. After 30 min of anoxia (NaN3, 2 mm), axonal membrane potential (V(m)) decreased to 42 +/- 11% of control and to 73 +/- 11% in the presence of tetrodotoxin (TTX) (1 microm). TTX + 4,4'-diisothiocyanatostilbene-2,2' disulfonic acid disodium salt (500 microm), a broad spectrum anion transport blocker, abolished anoxic depolarization (95 +/- 8%). Inhibition of the K-Cl cotransporter (KCC) (furosemide 100 microm) together with TTX was also more effective than TTX alone (84 +/- 14%). The compound action potential (CAP) area recovered to 26 +/- 6% of control after 1 hr anoxia. KCC blockade (10 microm furosemide) improved outcome (40 +/- 4%), and TTX (100 nm) was even more effective (74 +/- 12%). In contrast, the Cl- channel blocker niflumic acid (50 microm) worsened injury (6 +/- 1%). Coapplication of TTX (100 nm) + furosemide (10 microm) was more effective than either agent alone (91 +/- 9%). Furosemide was also very effective at normalizing the shape of the CAPs. The KCC3a isoform was localized to astrocytes. KCC3 and weaker KCC3a was detected in myelin of larger axons. KCC2 was seen in oligodendrocytes and within axon cylinders. Cl- gradients contribute to resting optic nerve membrane potential, and transporter and channel-mediated Cl- fluxes during anoxia contribute to injury, possibly because of cellular volume changes and disruption of axo-glial integrity, leading to propagation failure and distortion of fiber conduction velocities.
Indexed as
Identifiers
12736353PMC6742174W1627210966What 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.