ArticleMolecular pain2015
Transient, activity dependent inhibition of transmitter release from low threshold afferents mediated by GABAA receptors in spinal cord lamina III/IV.
Article in Molecular pain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 20 citations in OpenAlex.
- Presynaptic chloride-dependent regulation of spontaneous glutamate release in the rat medial preoptic nucleus.Frontiers in cellular neuroscience · 2026Article
- An electrophysiologist's guide to dorsal horn excitability and pain.Frontiers in cellular neuroscience · 2025Review
- Serotonergic 5-HTCurrent neuropharmacology · 2023Review
- Osteoporosis in Light of a New Mechanism Theory of Delayed Onset Muscle Soreness and Non-Contact Anterior Cruciate Ligament Injury.International journal of molecular sciences · 2022Article
- Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2Nature neuroscience · 2022Article
- Modulation of NMDA receptor activity by CR4056, an imidazoline-2 receptor ligand with analgesic properties.Frontiers in pain research (Lausanne, Switzerland) · 2022Article
- Spinal cord dorsal horn sensory gate in preclinical models of chemotherapy-induced painful neuropathy and contact dermatitis chronic itch becomes less leaky withFrontiers in molecular neuroscience · 2022Article
- 5-HTFrontiers in molecular neuroscience · 2022Article
- Presynaptic Inhibition of Pain and Touch in the Spinal Cord: From Receptors to Circuits.International journal of molecular sciences · 2021Review
- Mechanisms of Peripheral and Central Pain Sensitization: Focus on Ocular Pain.Frontiers in pharmacology · 2021Review
- Identification of a Potent and Selective 5-HTACS chemical neuroscience · 2020Article
- Chloride - The Underrated Ion in Nociceptors.Frontiers in neuroscience · 2020Review
- Pain Inhibits GRPR Neurons via GABAergic Signaling in the Spinal Cord.Scientific reports · 2019Article
- Serotonergic Modulation of Nociceptive Circuits in Spinal Cord Dorsal Horn.Current neuropharmacology · 2019Review
- Presynaptic Inhibition of Primary Nociceptive Signals to Dorsal Horn Lamina I Neurons by Dopamine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- GABAMolecular painArticle
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundPresynaptic GABAA receptors (GABAARs) located on central terminals of low threshold afferent fibers are thought to be involved in the processing of touch and possibly in the generation of tactile allodynia in chronic pain. These GABAARs mediate primary afferent depolarization (PAD) and modulate transmitter release. The objective of this study was to expand our understanding of the presynaptic inhibitory action of GABA released onto primary afferent central terminals following afferent stimulation.
resultsWe recorded evoked postsynaptic excitatory responses (eEPSCs and eEPSPs) from lamina III/IV neurons in spinal cord slices from juvenile rats (P17-P23, either sex), while stimulating dorsal roots. We investigated time and activity dependent changes in glutamate release from low threshold A fibers and the impact of these changes on excitatory drive. Blockade of GABAARs by gabazine potentiated the second eEPSC during a train of four afferent stimuli in a large subset of synapses. This resulted in a corresponding increase of action potential firing after the second stimulus. The potentiating effect of gabazine was due to inhibition of endogenously activated presynaptic GABAARs, because it was not prevented by the blockade of postsynaptic GABAARs through intracellular perfusion of CsF. Exogenous activation of presynaptic GABAARs by muscimol depressed evoked glutamate release at all synapses and increased paired pulse ratio (PPR).
conclusionsThese observations suggest that afferent driven release of GABA onto low threshold afferent terminals is most effective following the first action potential in a train and serves to suppress the initial strong excitatory drive onto dorsal horn circuitry.
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