title: Long-term cellular and regional specificity of the photoreceptor toxin, iodoacetic acid (IAA), in the rabbit retina.
abstract: This study investigated the anatomical consequences of a photoreceptor toxin, iodoacetic acid (IAA), in the rabbit retina. Retinae were examined 2 weeks, 1, 3, and 6 months after systemic IAA injection. The retinae were processed using standard histological methods to assess the gross morphology and topographical distribution of damage, and by immunohistochemistry to examine specific cell populations in the retina. Degeneration was restricted to the photoreceptors and was most common in the ventral retina and visual streak. In damaged regions, the outer nuclear layer was reduced in thickness or eliminated entirely, with a concomitant loss of immunoreactivity for rhodopsin. However, the magnitude of the effect varied between animals with the same IAA dose and survival time, suggesting individual differences in the bioavailability of the toxin. In all eyes, the inner retina remained intact, as judged by the thickness of the inner nuclear layer, and by the pattern of immunoreactivity for protein kinase C-alpha (rod bipolar cells) and calbindin D-28 (horizontal cells). Müller cell stalks became immunoreactive for glial fibrillary acidic protein (GFAP) even in IAA-treated retinae that had no signs of cell loss, indicating a response of the retina to the toxin. However, no marked hypertrophy or proliferation of Müller cells was observed with either GFAP or vimentin immunohistochemistry. Thus the selective, long lasting damage to the photoreceptors produced by this toxin did not lead to a reorganization of the surviving cells, at least with survival as long as 6 months, in contrast to the remodeling of the inner retina that is observed in inherited retinal degenerations such as retinitis pigmentosa and retinal injuries such as retinal detachment.
authors.affiliation: Department of Anatomy & Neurobiology, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
authors.forename: Li
authors.initials: L
authors.lastname: Liang
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Katagiri
authors.forename: Luisa M
authors.initials: LM
authors.lastname: Franco
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Yamauchi
authors.forename: Volker
authors.initials: V
authors.lastname: Enzmann
authors.forename: Henry J
authors.initials: HJ
authors.lastname: Kaplan
authors.forename: Julie H
authors.initials: JH
authors.lastname: Sandell
mesh_terms: D000818:Animals; D064026:Calbindins; D002467:Cell Nucleus / Q000473:pathology; D002470:Cell Survival / Q000187:drug effects; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007150:Immunohistochemistry; D007275:Injections, Intravenous; D019807:Iodoacetic Acid / Q000008:administration & dosage / Q000506:poisoning*; D009410:Nerve Degeneration / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology; D020419:Photoreceptor Cells, Vertebrate / Q000187:drug effects*; D051571:Protein Kinase C-alpha / Q000378:metabolism; D011817:Rabbits; D012160:Retina / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D051245:Retinal Bipolar Cells / Q000201:enzymology; D051248:Retinal Horizontal Cells / Q000378:metabolism; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D013997:Time Factors
chemical_list: D064026:Calbindins; D005904:Glial Fibrillary Acidic Protein; D064030:S100 Calcium Binding Protein G; D051571:Protein Kinase C-alpha; D019807:Iodoacetic Acid