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Spinal cord injury causes plasticity in a subpopulation of lamina I GABAergic interneurons
Journal article   Open access   Peer reviewed

Spinal cord injury causes plasticity in a subpopulation of lamina I GABAergic interneurons

Kimberly J. Dougherty and Shawn Hochman
Journal of neurophysiology, v 100(1)
01 Jul 2008
PMID: 18480373
url
https://doi.org/10.1152/jn.01104.2007View
Published, Version of Record (VoR)Open Access (License Unspecified) Open

Abstract

Life Sciences & Biomedicine Neurosciences Neurosciences & Neurology Physiology Science & Technology
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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