Spinal Cord Injury Causes Plasticity in a Subpopulation of Lamina I GABAergic Interneurons

J Neurophysiol. 2008 Jul;100(1):212-23. doi: 10.1152/jn.01104.2007. Epub 2008 May 14.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Cadmium / pharmacology
  • Calcium Channel Blockers / pharmacology
  • Disease Models, Animal
  • Dose-Response Relationship, Radiation
  • Electric Stimulation / methods
  • Glutamate Decarboxylase / genetics
  • Glutamate Decarboxylase / metabolism
  • Green Fluorescent Proteins / genetics
  • Green Fluorescent Proteins / metabolism
  • In Vitro Techniques
  • Interneurons / classification
  • Interneurons / physiology*
  • Membrane Potentials / genetics
  • Membrane Potentials / physiology
  • Membrane Potentials / radiation effects
  • Mice
  • Mice, Transgenic
  • Neuronal Plasticity / physiology*
  • Patch-Clamp Techniques / methods
  • Potassium Channel Blockers / pharmacology
  • Sodium Channel Blockers / pharmacology
  • Spinal Cord Injuries / pathology*
  • Spinal Cord Injuries / physiopathology*
  • Tetrodotoxin / pharmacology
  • gamma-Aminobutyric Acid / metabolism*


  • Calcium Channel Blockers
  • Potassium Channel Blockers
  • Sodium Channel Blockers
  • Cadmium
  • Green Fluorescent Proteins
  • Tetrodotoxin
  • gamma-Aminobutyric Acid
  • Glutamate Decarboxylase
  • glutamate decarboxylase 1