ArticleJournal of neurophysiology2008
Spinal cord injury causes plasticity in a subpopulation of lamina I GABAergic interneurons.
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 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Central Post-Stroke Pain: An Integrative Review of Somatotopic Damage, Clinical Symptoms, and Neurophysiological Measures.Frontiers in neurology · 2021Pooled it
- Plasticity in thoracic paravertebral sympathetic postganglionic neurons after high spinal cord transection.bioRxiv : the preprint server for biology · 2025Article
- Activity of spinal RORβ neurons is related to functional improvements following combination treatment after complete SCI.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- An electrophysiologist's guide to dorsal horn excitability and pain.Frontiers in cellular neuroscience · 2025Review
- Ionic Plasticity: Common Mechanistic Underpinnings of Pathology in Spinal Cord Injury and the Brain.Cells · 2022Review
- Review
- Identification of adult spinal Shox2 neuronal subpopulations based on unbiased computational clustering of electrophysiological properties.Frontiers in neural circuits · 2022Article
- Spinal Cord Injury Alters Spinal Shox2 Interneurons by Enhancing Excitatory Synaptic Input and Serotonergic Modulation While Maintaining Intrinsic Properties in Mouse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Bursting interneurons in the deep dorsal horn develop increased excitability and sensitivity to serotonin after chronic spinal injury.Journal of neurophysiology · 2020Article
- Metaplasticity within the spinal cord: Evidence brain-derived neurotrophic factor (BDNF), tumor necrosis factor (TNF), and alterations in GABA function (ionic plasticity) modulate pain and the capacity to learn.Neurobiology of learning and memory · 2018Article
- The Neuroplastic and Therapeutic Potential of Spinal Interneurons in the Injured Spinal Cord.Trends in neurosciences · 2018Review
- Ionic plasticity and pain: The loss of descending serotonergic fibers after spinal cord injury transforms how GABA affects pain.Experimental neurology · 2018Article
- Calcium signalling through L-type calcium channels: role in pathophysiology of spinal nociceptive transmission.British journal of pharmacology · 2018Review
- When Pain Hurts: Nociceptive Stimulation Induces a State of Maladaptive Plasticity and Impairs Recovery after Spinal Cord Injury.Journal of neurotrauma · 2017Review
- Spatiotemporal correlation of spinal network dynamics underlying spasms in chronic spinalized mice.eLife · 2017Article
- Acute spinal cord injury (SCI) transforms how GABA affects nociceptive sensitization.Experimental neurology · 2016Article
- Immature spinal cord neurons are dynamic regulators of adult nociceptive sensitivity.Journal of cellular and molecular medicine · 2015Article
- Functional alterations in GABAergic fast-spiking interneurons in chronically injured epileptogenic neocortex.Neurobiology of disease · 2012Article
- Pacemaker neurons within newborn spinal pain circuits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Dysfunction of the spinal GABAergic system has been implicated in pain syndromes following spinal cord injury (SCI). Since lamina I is involved in nociceptive and thermal signaling, we characterized the effects of chronic SCI on the cellular properties of its GABAergic neurons fluorescently identified in spinal slices from GAD67-GFP transgenic mice. Whole cell recordings were obtained from the lumbar cord of 13- to 17-day-old mice, including those having had a thoracic segment (T8-11) removed 6-9 days prior to experiments. Following chronic SCI, the distribution, incidence, and firing classes of GFP+ cells remained similar to controls, and there were minimal changes in membrane properties in cells that responded to current injection with a single spike. In contrast, cells displaying tonic/initial burst firing had more depolarized membrane potentials, increased steady-state outward currents, and increased spike heights. Moreover, higher firing frequencies and spontaneous plateau potentials were much more prevalent after chronic SCI, and these changes occurred predominantly in cells displaying a tonic firing pattern. Persistent inward currents (PICs) were observed in a similar fraction of cells from spinal transects and may have contributed to these plateaus. Persistent Na+ and L-type Ca2+ channels likely contributed to the currents as both were identified pharmacologically. In conclusion, chronic SCI induces a plastic response in a subpopulation of lamina I GABAergic interneurons. Alterations are directed toward amplifying neuronal responsiveness. How these changes alter spinal sensory integration and whether they contribute to sensory dysfunction remains to be elucidated.
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