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N. Zabouri, M.–L. Garon, F. Huppé–Gourgues, A.L. Dorfman, S. Chemtob, P. Lachapelle, C. Casanova; Oxygen–Induced Retinopathy in Neonatal Rats: Evidence for Postretinal Sequels . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3443.
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Purpose: : Postnatal hyperoxia causes irreversible structural and functional damage to the retina of newborn Sprague–Dawley (SD) rats. The present study investigates the impact of the hyperoxia–induced retinal dysfunction on visual responses in the superior colliculus (SC), a prominent direct target of retinal ganglion cells. Methods: Newborn SD rats were exposed to hyperoxic conditions as previously described (Dorfman et al., IOVS, 44: E–Abstract 1873, 2003). Once they reached their adult age, ocular injections of the beta subunit of cholera toxin (CTB) were performed in order to quantify the terminal boutons at the level of the SC. In addition, carbon–fiber electrodes (impedance ≤ 1MΩ) were used to record visual evoked potentials (VEPs – bandwidth 1–300Hz) in the colliculus as a function of depth. Results: The CTB injections revealed that the absolute density of ganglion fiber endings was similar in hyperoxic and normoxic rats. However, the number of terminal boutons appeared to be reduced in the SC of hyperoxic rats. In control rats, the intra–collicular VEP signal included an early (30ms latency) biphasic potential, followed by a late positive waveform of smaller amplitude (latency of 120 msec). In exposed animals, the early waveform was strongly reduced while the amplitude and latency of the late potentials were increased. Moreover, in the exposed rats only, the latency of the late waveform increased with collicular depth (difference of 30 ms between superficial and deep VEPs). Conclusions: These results suggest that the hyperoxia–induced changes observed at the level of the SC, such as the absence of short latency waveforms, may be explained in part by the direct consequence of an abnormal retinal function and/or an abnormal retinofugal pathway (as suggested by the reduction of ganglion cells terminal boutons). In addition, the modified latency VEP waveform and the delay between dorsal and ventral responses support the possibility of an altered processing of visual signals within the SC of neonatal hyperoxia exposed rats.
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