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O. R. Neaga, J. Racine, A. Polosa, P. Lachapelle; Evidence Suggesting a Central Retinal Anomaly in Our Night Blind Guinea Pigs. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2213.
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We have previously reported guinea pigs affected with a night blinding disorder characterized with a complete absence of rod receptors and relatively well-preserved cones. The purpose of our study was to further our understanding of the retinal and retinofugal functions of this unique animal model.
Photopic flash ERGs [(fERG); flash: 0.9 log cd.s.m-2; background: 30 cd.m-2; bandwidth: 1-1000 Hz)], multifocal ERGs and OPs [37 hexagons; white: 200 cd.m-2; black: 0 cd.m-2; background: 100 cd.m-2; bandwidth: 10-100 Hz (mfERG) and 100-300 Hz (mfOPs)] and flash VEPs [(fVEPs); flash: 0.9 log cd.s.m-2; background: 30 cd.m-2; bandwidth: 1-1000 Hz)] were obtained from normal and night blind guinea pigs (NBGP) aged 2 months old.
(Values are in uVolts). The amplitude of the fERG a-wave was significantly reduced in our NBGP compared to normal (NBGP: 11.0 ± 2.5; normal: 37.8 ± 5.5; ρ<0.05). In contrast, b-wave amplitudes were not significantly different from normal (normal: 90.4 ± 9.1; NBGP: 79.0 ± 11.9; ρ>0.05). However both a- and b-waves were of normal timing. Of further interest, an i-wave (post b-wave component) could not be recorded from our NBGP. mfERG and mfOPs were both significantly attenuated in our NBGP, irrespective of hexagon location. While 4 major positive waves (P1-P4) usually characterize the fVEPs of normal guinea pigs only 3 could be elicited from our NBGP (wave 4 missing). Wave 1 was significantly larger in NBGP compared to normal (NBGP: 5.4 ± 1.2; normal: 3.2 ± 1.2; ρ>0.05), whereas wave 2 (normal: 20.5 ± 6.8; NBGP: 10.2 ± 5.8; ρ<0.05) and wave 3 (normal: 33.2 ± 5.0; NBGP: 17.8 ± 6.7; ρ<0.05) were significantly attenuated. Peak times were also significantly delayed in our NBGP by an average 5 msec (ρ<0.05).
Despite a relatively normal photopic fERG our NBGP disclosed significant anomaly at the mfERG as well significant amplitude and peak time delays at the fVEP. These results would thus suggest an impaired central retina with possible repercussion at the visual cortex unless the abnormal fVEP results from the lack of a rod contribution. Supported by CIHR and FRSQ vision network.
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