ArticleNeuroscience2012
Persistent inflammation increases GABA-induced depolarization of rat cutaneous dorsal root ganglion neurons in vitro.
Article in Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Development of a Novel Benzodiazepine to Delineate Peripheral GABA-A Signaling Mechanisms in Visceral Pain Syndromes.Cellular and molecular gastroenterology and hepatology · 2026Article
- Depolarization of mouse DRG neurons by GABA does not translate into acute pain or hyperalgesia in healthy human volunteers.PloS one · 2024Article
- Autonomic control of ventricular function in health and disease: current state of the art.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023Review
- Pre-Synaptic GABACells · 2022Article
- Understanding Lung Carcinogenesis from a Morphostatic Perspective: Prevention and Therapeutic Potential of Phytochemicals for Targeting Cancer Stem Cells.International journal of molecular sciences · 2021Review
- Neuropathic Injury-Induced Plasticity of GABAergic System in Peripheral Sensory Ganglia.Frontiers in pharmacology · 2021Article
- Chloride - The Underrated Ion in Nociceptors.Frontiers in neuroscience · 2020Review
- The antinociceptive effect of artemisinin on the inflammatory pain and role of GABAergic and opioidergic systems.The Korean journal of pain · 2019Article
- Acute inflammation sensitizes knee-innervating sensory neurons and decreases mouse digging behavior in a TRPV1-dependent manner.Neuropharmacology · 2018Article
- Review
- Adult Mouse DRG Explant and Dissociated Cell Models to Investigate Neuroplasticity and Responses to Environmental Insults Including Viral Infection.Journal of visualized experiments : JoVE · 2018Article
- Transcriptomes and neurotransmitter profiles of classes of gustatory and somatosensory neurons in the geniculate ganglion.Nature communications · 2017Article
- Local GABAergic signaling within sensory ganglia controls peripheral nociceptive transmission.The Journal of clinical investigation · 2017Article
- Acute inflammation reveals GABAPhysiological reports · 2017Article
- Combined Changes in Chloride Regulation and Neuronal Excitability Enable Primary Afferent Depolarization to Elicit Spiking without Compromising its Inhibitory Effects.PLoS computational biology · 2016Article
- Inflammatory mediator-induced modulation of GABAA currents in human sensory neurons.Neuroscience · 2015Article
- Redox and trace metal regulation of ion channels in the pain pathway.The Biochemical journal · 2015Review
- Experimental and computational evidence for an essential role of NaV1.6 in spike initiation at stretch-sensitive colorectal afferent endings.Journal of neurophysiology · 2015Article
- When GABA Fails: Rundown on Chemokines.Epilepsy currents · 2014Article
- Activity-dependent hyperpolarization of EGABA is absent in cutaneous DRG neurons from inflamed rats.Neuroscience · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Persistent inflammation is associated with a shift in spinal GABA(A) signaling from inhibition to excitation such that GABA(A)-receptor activation contributes to inflammatory hyperalgesia. We tested the hypothesis that the primary afferent is the site of the persistent inflammation-induced shift in GABA(A) signaling which is due to a Na(+)-K(+)-Cl(-)-co-transporter (NKCC1)-dependent depolarization of the GABA(A) current equilibrium potential (E(GABA)). Acutely dissociated retrogradely labeled cutaneous dorsal root ganglion (DRG) neurons from naïve and inflamed (3 days after a subcutaneous injection of complete Freund's adjuvant) adult male rats were studied with Ca(2+) imaging, western blot and gramicidin-perforated patch recording. GABA evoked a Ca(2+) transient in a subpopulation of small- to medium-diameter capsaicin-sensitive cutaneous neurons. Inflammation was associated with a significant increase in the magnitude of GABA-induced depolarization as well as the percentage of neurons in which GABA evoked a Ca(2+) transient. There was no detectable change in NKCC1 protein or phosphoprotein at the whole ganglia level. Furthermore, the increase in excitatory response was comparable in both HEPES- and HCO(3)(-)-buffered solutions, but was only associated with a depolarization of E(GABA) in HCO(3)(-)-based solution. In contrast, under both recording conditions, the excitatory response was associated with an increase in GABA(A) current density, a decrease in low threshold K(+) current density, and resting membrane potential depolarization. Our results suggest that increasing K(+) conductance in afferents innervating a site of persistent inflammation may have greater efficacy in the inhibition of inflammatory hyperalgesia than attempting to drive a hyperpolarizing shift in E(GABA).
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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.