Premium
Prenatal hypoxia causes long‐term retina dysfunction in rats
Author(s) -
Bourque Stephane Louis,
Kuny Sharee,
Sauve Yves,
Davidge Sandra T
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1178.4
Subject(s) - offspring , retina , hypoxia (environmental) , electroretinography , fetus , biology , endocrinology , erg , medicine , physiology , pregnancy , neuroscience , chemistry , genetics , organic chemistry , oxygen
Background Evidence indicates that prenatal stressors, such as hypoxia, can induce phenotypic changes in the fetus which increase its predisposition to age‐related complications. We hypothesized that aged offspring exposed to prenatal hypoxia would exhibit exacerbated age‐related functional decline of the retina. Methods Female Sprague‐Dawley rat offspring (that were maintained at either 11% O 2 [hypoxic] or 21% O 2 [normoxic] from gestational day (GD)15 to GD21, term=GD22) had their retina function assessed 2 and 14 months of age by electroretinophy (ERG). Anatomy was assessed by immunofluorescence microscopy. Results Dark‐adapted mixed a‐wave (rod and cone function) and b‐wave (bipolar cell activity) amplitudes were diminished in hypoxic offspring; these effects were most apparent at 14 months. Young and aged hypoxic offspring also had fewer mixed a‐wave threshold responses, and mixed b‐wave responses were markedly reduced in light adapted conditions. Light‐adapted flicker fusion frequency was also reduced in aged hypoxic versus age‐matched normoxic controls. There was no evidence of reduced photoreceptor cell numbers, although there was evidence of glial fibrillary acidic protein (GFAP) accumulation in aged IUGR offspring, providing evidence of photoreceptor damage. Conclusions Prenatal hypoxia causes both intrinsic and age‐related changes in retina function.