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Keywords:

  • ischemia;
  • reperfusion;
  • amino acids;
  • pattern recognition;
  • agmatine;
  • cation channels;
  • glutamate;
  • excitotoxicity;
  • immunocytochemistry

Abstract

We quantitatively tracked the recovery in amino acid labeling and cation channel functionality within distinct retinal elements for up to 2 weeks after an ischemic insult. Pattern recognition analysis of multiple amino acid and agmatine (a cation channel probe; 1-amino-4-guanidobutane; AGB) immunocytochemical patterns was used to classify all neural elements within the retina. This classification was spatially complete and with single-cell resolution. By 48 hours of reperfusion the amino acid labeling pattern of virtually all cell populations had returned to near preischemic levels, with the exception of glutamine and alanine levels, which remained significantly higher in many cell populations. Classification resulted in a total of 18 statistically separable theme classes (including neurons, glia, and extraretinal classes), a reduction of 10 theme classes from the normal retina (Sun et al. [ 2007a, b] J Comp Neurol, this issue). In addition to the known selective losses of amacrine cell types within the inner nuclear layer, we now demonstrate a selective loss of theme classes representing cone bipolar cells within the bipolar cell population. While there was a recovery in the amino acid labeling pattern, there were persistent cation channel gating anomalies (as reflected by AGB labeling) within several theme classes, including the theme class representing all the remaining rod bipolar cells, suggesting aberrant neuronal function secondary to metabolic insult. J. Comp. Neurol. 505:114–130, 2007. © 2007 Wiley-Liss, Inc.