title: The retinal anatomy and function of the myelin mutant taiep rat.
abstract: OBJECTIVE
  To study the histology and the physiological function of the retina in the neurological myelin mutant, taiep rats during the postnatal developmental period (P20-P360).
  
  
  METHODS
  Electroretinography (ERG) was applied to evaluate intensity dependence and spectral sensitivity of the responses to light. Retinal histology, morphometry, and immunocytochemistry were used to characterize the structure of the retina, with particular emphasis on the Müller (glial) cells.
  
  
  RESULTS
  In the taiep rats of all ages studied, the scotopic ERG showed normal a- and b-wave amplitudes and latencies; likewise, the scotopic spectral sensitivity function was the same for control and taiep animals, with a maximal sensitivity (lambda(max)) at 500 nm. However, in adult taiep rats (P90 to P360) a secondary cornea-positive wave ('b(2)') was observed in response to high stimulus intensities, which never occurred in controls. This correlated with the observation that in the photopic ERG responses of the taiep rats, the b-wave was reduced in amplitude, and was followed by a rapid cornea-negative after-potential. After 1 year of life, in taiep rats the outer plexiform layer (OPL) became slightly thinner and the inner plexiform/ganglion cell layers (IPL/GCL) appeared to be swollen, and increased in thickness; in addition, the number of retinal neurons (particularly, of photoreceptor cells) slightly decreased. Increased GFAP immunoreactivity revealed a hypertrophy and reactivity of the Müller cells in 1-year-old taiep rats.
  
  
  CONCLUSIONS
  The present results suggest the occurrence of a relatively mild and slowly progressing neural retinal alteration in taiep rats, which becomes histologically and functionally evident at the end of the first year of life, and mainly affects the circuit(s) of the photopic ON-response. It is speculated that this alteration is due to missing/altered signals from demyelinated optic nerve.
authors.affiliation: Molecular Cellular Center for Neuroscience of Valparaiso, Faculty of Science, University of Valparaíso, P.O. Box 5030, Valparaíso, Chile.
authors.forename: Andrés E
authors.initials: AE
authors.lastname: Chávez
authors.forename: Manuel
authors.initials: M
authors.lastname: Roncagliolo
authors.forename: Heidrun
authors.initials: H
authors.lastname: Kuhrt
authors.forename: Andreas
authors.initials: A
authors.lastname: Reichenbach
authors.forename: Adrián G
authors.initials: AG
authors.lastname: Palacios
mesh_terms: D000221:Adaptation, Ocular / Q000502:physiology; D000367:Age Factors; D000818:Animals; D004596:Electroretinography; D005904:Glial Fibrillary Acidic Protein; D007150:Immunohistochemistry; D008564:Membrane Potentials / Q000502:physiology; D009186:Myelin Sheath / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D009410:Nerve Degeneration / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D009457:Neuroglia / Q000378:metabolism* / Q000473:pathology; D009900:Optic Nerve / Q000254:growth & development* / Q000378:metabolism / Q000473:pathology; D010775:Photic Stimulation; D010786:Photoreceptor Cells / Q000254:growth & development / Q000473:pathology / Q000503:physiopathology; D011237:Predictive Value of Tests; D051381:Rats; D011922:Rats, Mutant Strains; D012160:Retina / Q000254:growth & development* / Q000378:metabolism / Q000473:pathology; D012164:Retinal Diseases / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D012165:Retinal Ganglion Cells / Q000378:metabolism / Q000473:pathology
chemical_list: D005904:Glial Fibrillary Acidic Protein