Dexamethasone-coated neural probes elicit attenuated inflammatory response and neuronal loss compared to uncoated neural probes

Brain Res. 2007 May 7;1148:15-27. doi: 10.1016/j.brainres.2007.02.024. Epub 2007 Feb 22.


Glial scar formation around implanted silicon neural probes compromises their ability to facilitate long-term recordings. One approach to modulate the tissue reaction around implanted probes in the brain is to develop probe coatings that locally release anti-inflammatory drugs. In this study, we developed a nitrocellulose-based coating for the local delivery of the anti-inflammatory drug dexamethasone (DEX). Silicon neural probes with and without nitrocellulose-DEX coatings were implanted into rat brains, and inflammatory response was evaluated 1 week and 4 weeks post implantation. DEX coatings significantly reduced the reactivity of microglia and macrophages 1 week post implantation as evidenced by ED1 immunostaining. CS56 staining demonstrated that DEX treatment significantly reduced chondroitin sulfate proteoglycan (CSPG) expression 1 week post implantation. Both at 1-week and at 4-week time points, GFAP staining for reactive astrocytes and neurofilament (NF) staining revealed that local DEX treatment significantly attenuated astroglial response and reduced neuronal loss in the vicinity of the probes. Weak ED1, neurocan, and NG2-positive signal was detected 4 weeks post implantation for both coated and uncoated probes, suggesting a stabilization of the inflammatory response over time in this implant model. In conclusion, this study demonstrates that the nitrocellulose-DEX coating can effectively attenuate the inflammatory response to the implanted neural probes, and reduce neuronal loss in the vicinity of the coated probes. Thus anti-inflammatory probe coatings may represent a promising approach to attenuate astroglial scar and reduce neural loss around implanted neural probes.

Publication types

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

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Anti-Inflammatory Agents / therapeutic use
  • Astrocytes / drug effects*
  • Astrocytes / physiology
  • Biomarkers / metabolism
  • Chondroitin Sulfates / metabolism
  • Collodion / therapeutic use
  • Dexamethasone / pharmacology*
  • Dexamethasone / therapeutic use
  • Ectodysplasins / drug effects
  • Ectodysplasins / metabolism
  • Electrodes, Implanted / adverse effects
  • Encephalitis / drug therapy*
  • Encephalitis / physiopathology
  • Encephalitis / prevention & control
  • Glial Fibrillary Acidic Protein / drug effects
  • Glial Fibrillary Acidic Protein / metabolism
  • Gliosis / drug therapy*
  • Gliosis / physiopathology
  • Gliosis / prevention & control
  • Infusion Pumps, Implantable / trends
  • Macrophages / drug effects
  • Macrophages / physiology
  • Male
  • Microglia / drug effects
  • Microglia / physiology
  • Nerve Degeneration / drug therapy*
  • Nerve Degeneration / physiopathology
  • Nerve Degeneration / prevention & control
  • Nerve Tissue Proteins / drug effects
  • Nerve Tissue Proteins / metabolism
  • Neurofilament Proteins / drug effects
  • Neurofilament Proteins / metabolism
  • Proteoglycans / drug effects
  • Proteoglycans / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Treatment Outcome


  • Anti-Inflammatory Agents
  • Biomarkers
  • Ectodysplasins
  • Eda protein, mouse
  • Glial Fibrillary Acidic Protein
  • Ncan protein, mouse
  • Nerve Tissue Proteins
  • Neurofilament Proteins
  • Proteoglycans
  • Dexamethasone
  • Collodion
  • Chondroitin Sulfates