ArticleProceedings. Biological sciences1999
Low expression of the ClC-2 chloride channel during postnatal development: a mechanism for the paradoxical depolarizing action of GABA and glycine in the hippocampus.
Article in Proceedings. Biological sciences, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- Glial Chloride Channels in the Function of the Nervous System Across Species.Advances in experimental medicine and biology · 2021Article
- Components of neuronal chloride transport in rat and human neocortex.The Journal of physiology · 2011Article
- Mutations affecting GABAergic signaling in seizures and epilepsy.Pflugers Archiv : European journal of physiology · 2010Review
- ClC-2 voltage-gated channels constitute part of the background conductance and assist chloride extrusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- The specification of glycinergic neurons and the role of glycinergic transmission in development.Frontiers in molecular neuroscience · 2010Article
- GABA(A) receptors in normal development and seizures: friends or foes?Current neuropharmacology · 2008Article
- Mutations in the CLCN2 gene are a rare cause of idiopathic generalized epilepsy syndromes.Neurogenetics · 2006Article
- Putative ClC-2 chloride channel mediates inward rectification in Drosophila retinal photoreceptors.The Journal of membrane biology · 2005Article
- Differential expression of genes at stages when regeneration can and cannot occur after injury to immature mammalian spinal cord.Cellular and molecular neurobiology · 2005Article
- Stiff Goats, Chloride Ions, and Idiopathic Generalized Epilepsy (IGE).Epilepsy currents · 2003Article
- Inward-rectifying anion channels are expressed in the epithelial cells of choroid plexus isolated from ClC-2 'knock-out' mice.The Journal of physiology · 2002Article
- Antioxidant N-acetylcysteine modifies the purinergic modulation of spontaneous postsynaptic potentials in the newborn rat hippocampus.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sectionsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In early postnatal development, during the period of synapse formation, gamma-aminobutyric acid (GABA) and glycine, the main inhibitory transmitters in the adult brain, paradoxically excite and depolarize neuronal membranes by an outward flux of chloride. The mechanisms of chloride homeostasis are not fully understood. It is known that in adult neurons intracellular chloride accumulation is prevented by a particular type of chloride channel, the ClC-2. This channel strongly rectifies in the inward direction at potentials negative to ECl thus ensuring chloride efflux. We have tested the hypothesis that in the developing hippocampus, a differential expression or regulation of ClC-2 channels may contribute to the depolarizing action of GABA and glycine. We have cloned a truncated form of ClC-2 (ClC-2nh) from the neonatal hippocampus which lacks the 157 bp corresponding to exon 2. In situ hybridization experiments show that ClC-2nh is the predominant form of ClC-2 mRNA in the neonatal brain. ClC-2nh mRNA is unable to encode a full-length protein due to a frameshift, consequently it does not induce any currents upon injection into Xenopus oocytes. Low expression of the full-length ClC-2 channel, could alter chloride homeostasis, lead to accumulation of [Cl-]i and thereby contribute to the depolarizing action of GABA and glycine during early development.
Indexed as
Identifiers
What 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.