ArticleJournal of neurophysiology2008
Na+,K+,2Cl- cotransport and intracellular chloride regulation in rat primary sensory neurons: thermodynamic and kinetic aspects.
Article in Journal of neurophysiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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.
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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.
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Who cites it
49 citing papers in PubMed, 93 citations in OpenAlex.
- ClC-2 Contributes to Hypotonicity-Induced Adrenal Aldosterone Secretion.Acta physiologica (Oxford, England) · 2026Article
- Molecular Anatomy of Synaptic and Extrasynaptic Neurotransmission Between Nociceptive Primary Afferents and Spinal Dorsal Horn Neurons.International journal of molecular sciences · 2025Review
- Article
- GABA Type A receptors expressed in triple negative breast cancer cells mediate chloride ion flux.Frontiers in pharmacology · 2024Article
- Bumetanide increases postsynaptic inhibition after chronic SCI and decreases presynaptic inhibition with step-training.The Journal of physiology · 2023Article
- Synchronous firing of dorsal horn neurons at the origin of dorsal root reflexes in naïve and paw-inflamed mice.Frontiers in cellular neuroscience · 2022Article
- The Role of TMEM16A/ERK/NK-1 Signaling in Dorsal Root Ganglia Neurons in the Development of Neuropathic Pain Induced by Spared Nerve Injury (SNI).Molecular neurobiology · 2021Article
- Nicotinic receptor modulation of primary afferent excitability with selective regulation of Aδ-mediated spinal actions.Journal of neurophysiology · 2021Article
- Presynaptic Inhibition of Pain and Touch in the Spinal Cord: From Receptors to Circuits.International journal of molecular sciences · 2021Review
- The Role of Thermosensitive Ion Channels in Mammalian Thermoregulation.Advances in experimental medicine and biology · 2021Article
- Differential expression of NaScientific reports · 2020Article
- Novel Analgesics with Peripheral Targets.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- Reviewing the case for compromised spinal inhibition in neuropathic pain.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- OEsophageal Ion Transport Mechanisms and Significance Under Pathological Conditions.Frontiers in physiology · 2020Review
- Physiological Processes Modulated by the Chloride-Sensitive WNK-SPAK/OSR1 Kinase Signaling Pathway and the Cation-Coupled Chloride Cotransporters.Frontiers in physiology · 2020Review
- Chloride - The Underrated Ion in Nociceptors.Frontiers in neuroscience · 2020Review
- Genetic and pharmacological inactivation of apical NaAmerican journal of physiology. Cell physiology · 2019Article
- Identification of Chloride Channels CLCN3 and CLCN5 Mediating the Excitatory ClFrontiers in molecular neuroscience · 2018Article
- ClJournal of neurophysiology · 2017Article
- The neuronal KScientific reports · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Adult primary afferent neurons are depolarized by GABA throughout their entire surface, including their somata located in dorsal root ganglia (DRG). Primary afferent depolarization (PAD) mediated by GABA released from spinal interneurons determines presynaptic inhibition, a key mechanism in somatosensory processing. The depolarization is due to Cl(-) efflux through GABA(A) channels; the outward Cl(-) gradient is generated by a Na+,K+,2Cl(-) cotransporter (NKCC) as first established in amphibians. Using fluorescence imaging microscopy we measured [Cl(-)]i and cell water volume (CWV) in dissociated rat DRG cells (P0-P21) loaded with N-(ethoxycarbonylmethyl)-6-methoxyquinolinium bromide and calcein, respectively. Basal [Cl(-)]i was 44.2 +/- 1.2 mM (mean +/- SE), Cl(-) equilibrium potential (E Cl) was -27.0 +/- 0.7 mV (n = 75). This [Cl(-)]i is about four times higher than electrochemical equilibrium. On isosmotic removal of external Cl(-), cells lost Cl(-) and shrank. On returning to control solution, cells reaccumulated Cl(-) and recovered CWV. Cl(-) reaccumulation had Na+-dependent (SDC) and Na+-independent (SIC) components. The SIC stabilized at [Cl(-)]i = 13.2 +/- 1.2 mM, suggesting that it was passive (E(Cl) = -60.5 +/- 3 mV). Bumetanide blocked CWV recovery and most (65%) of the SDC (IC50 = 5.7 microM), indicating that both were mediated by NKCC. Active Cl(-) uptake fell with increasing [Cl(-)]i and became negligible when [Cl(-)]i reached basal levels. The kinetics of active Cl(-) uptake suggests a negative feedback system in which intracellular Cl(-)regulates its own influx thereby keeping [Cl(-)]i constant, above electrochemical equilibrium but below the value that would attain if NKCC reached thermodynamic equilibrium.
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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.