Studies of
retinal ischemia/reperfusion indicate a disparity between the anatomical and functional results; while a large number of rod bipolar cells remain postischemia, there is a significant reduction in the amplitude of the scotopic b-wave of the electroretinogram (ERG). We investigated the alterations in photoreceptor-bipolar cell signaling following
ischemia/reperfusion and suggest a mechanism for the decrease in b-wave amplitude. A
cation channel probe (agmatine, 1-amino-4-guanidobutane, AGB) was used to assess cellular
ion channel activity in neurochemically identified cells secondary to endogenous
glutamate release or pharmacological manipulations. By applying the "neurochemical truth point" principle (Sun et al. [2007a] J Comp Neurol, this issue), we have been able to confirm the loss of specific subpopulations of neurons. ERG was used to assess gross
retinal function, with parameters of the ERG model providing insight into changes in the phototransduction cascade and sensitivity of postreceptoral
glutamate receptors. Following
ischemia/reperfusion, rod bipolar cells maintained
2-amino-4-phosphonobutyric acid-responsive
metabotropic glutamate receptors and displayed no change in sensitivity to flashes of light as assessed by ERG. Therefore, the loss in b-wave amplitude is likely due to alterations in photoreceptoral
glutamate release detected as a change in postsynaptic AGB permeation into rod bipolar cells. Bipolar cell to amacrine cell signaling was also altered. The robust AGB entry into
cholinergic amacrine cells was virtually absent in retinas that had undergone
ischemia/reperfusion but remained in the AII amacrine cells. Such results suggest a loss of
glutamate receptors and/or a change in receptor subunit expression in subpopulations of inner retinal neurons. Although many cells retain their characteristic neurochemical labeling following
ischemia/reperfusion, caution should be used when assuming cells participate in functional
retinal circuits based solely on the persistence of neurochemical labeling.