title: Alterations in photoreceptor-bipolar cell signaling following ischemia/reperfusion in the rat retina.
abstract: 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.
authors.affiliation: Department of Optometry and Vision Science, University of Auckland, New Zealand.
authors.forename: Daniel
authors.initials: D
authors.lastname: Sun
authors.forename: Bang V
authors.initials: BV
authors.lastname: Bui
authors.forename: Algis J
authors.initials: AJ
authors.lastname: Vingrys
authors.forename: Michael
authors.initials: M
authors.lastname: Kalloniatis
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D002452:Cell Count; D004596:Electroretinography / Q000379:methods; D066298:In Vitro Techniques; D009419:Nerve Tissue Proteins / Q000378:metabolism; D010786:Photoreceptor Cells / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology*; D012160:Retina / Q000473:pathology*; D051245:Retinal Bipolar Cells / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*; D013997:Time Factors
chemical_list: D009419:Nerve Tissue Proteins