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B.V. Bui, B. Fortune; Origin of Electroretinogram Amplitude Growth During Light Adaptation in Rat . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2250.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To characterize the growth of the rat photopic electroretinogram (ERG) during light adaptation and to evaluate the mechanisms underlying this process. Methods: Full field ERG responses were recorded from both eyes of Brown–Norway rats (age 10 – 12 weeks) under ketamine : xylazine : acepromazine anesthesia, (30 : 2 : 1 mg/kg) each minute for 20 minutes of light adaptation on 3 background intensities (150, 75, 37.5 cd m–2). After 30 minutes, an intensity–response function was obtained (0.97 to 2.7 log cd s m–2). The course of light adaptation was also assessed after intravitreal injection of pharmacological agents that block inner retinal responses, including TTX (1.2 – 8 µM, n = 5), CNQX/D–AP7 (200 µM/200 µM, n = 4), CNQX/L–AP4 (200 µM/1 mM, n = 5) and PDA/L–AP4 (5 mM/1 mM, n = 3). ERGs were band passed filtered (30 – 170 Hz) to extract the oscillatory potentials (OPs) for summed amplitude measurements. OPs were digitally subtracted from the ERG prior to measurement of b–wave amplitude and implicit time. Results: The rat photopic b–wave amplitude increased with duration of light adaptation (baseline, 236 ± 25 µV vs. 20 min, 351 ± 16 µV) and its width at 33% maximal amplitude narrowed (baseline, 142 ± 7 ms vs. 20 min, 97 ± 4 ms). These effects peaked 12 – 15 minutes after background onset. The narrowing of the b–wave reflected steepening of the b–wave recovery phase, with little change in the rising phase. OP amplitudes grew in proportion to the b–wave. Inhibition of inner retinal responses using TTX resulted in a greater relative b–wave and OP growth compared with fellow control eyes (229 ± 43% vs. 72 ± 9%) and delayed the change in recovery phase by ∼5 min. Inhibition of all ionotropic glutamate receptors with CNQX/D–AP7 delayed both rising and recovery phases equally (∼10 ms) without altering b–wave width or the time course of adaptation changes. The full photopic cone a–wave was exposed using PDA/L–AP4 or CNQX/L–AP4. A–wave amplitude (at 35 ms criterion) also increased with light adaptation and reached a maximum (130 ± 29% above baseline) 12 – 15 minutes after background onset. B–wave amplitude growth in fellow control eyes closely followed the course and relative magnitude of cone a–wave amplitude growth. Conclusions: The increase of the cone photoresponse during light adaptation is sufficient to explain b–wave amplitude growth. Inner retinal light responses are not directly responsible for b–wave amplitude growth, but may contribute to the change in its recovery phase during adaptation. A TTX–sensitive mechanism, perhaps dopamine release, may help to hasten this process.
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