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Origins of the Primate Flicker ERG: Distal versus Proximal Retinal Generators
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Benedetto Falsini, MD (1) and Vittorio Porciatti, ScDr (2) (1) Istituto di Oftalmologia, Universita' Cattolica (2) Bascom Palmer Eye Institute, Univ. of Miami
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md0571{at}mclink.it Benedetto Falsini, MD (1) and Vittorio Porciatti, ScDr (2)
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In the recent article by Kondo and Sieving1 on the origin of the primate Ganzfeld flicker ERG, the authors evaluated the ON- and OFF-postreceptoral contribution to the fundamental harmonic response component, after isolation by glutamate analogs. They concluded that both ON- and OFF-postreceptoral generators contribute predominantly to the ERG fundamental component to high-frequency stimuli, whereas a photoreceptoral contribution is dominant in the ERG fundamentals elicited by frequencies equal or less than 10 Hz. They reported, referring to previous clinical studies of our group,2,3 that their findings in the primate "cast doubt on using the (ERG) fundamental and second harmonic components to deduce photoreceptor versus inner retinal activity." Given the clinical implications2,3 of the Kondo and Sieving1 paper, we feel that some issues, related to the interpretation of results, need to be brought to the authors' attention. First, some caution is necessary when relating Ganzfeld ERGs data from anesthetized monkeys to results obtained with focal (macular) stimulation in human patients, as we did in our previous studies.2-4 A change in the relative contribution of response generators to the macular as compared to the Ganzfeld response cannot be excluded. Second, Kondo and Sieving1 did not evaluate the flicker ERG second harmonic, which is well represented in their Figure 2 for frequencies of 10 Hz or less (see below). It is now well supported by work with monkeys5,6 and humans7,8 that the flicker ERG second harmonic, recorded at frequencies less than 10 Hz, is generated more proximally with respect to the ERG fundamental. Even assuming that the human fundamental at high, but not at low frequencies is dominated by postreceptoral activity, the proximal origin of the second harmonic still supports the clinical use of fundamental and second harmonic as probes of distal and proximal retinal activity, respectively. Kondo and Sieving did not show the second harmonic ERG data, but it is apparent from Figure 2 of their paper1 that, at low frequencies (10 Hz or less), the second harmonic gives a substantial contribution to the control ERG. In addition, the second harmonic loss after APB administration is by far greater than that of the fundamental, implying that even in the Kondo and Sieving1 monkey model the dichotomy applies. Finally, we would like to stress that in the clinical studies of our group, the ERG fundamental was recorded not only at high frequencies (32 Hz) but also at 8 Hz. In patients with different kinds of retinal dysfunctions,9 losses in the 8 Hz fundamental were similar to those in the 32 Hz fundamental, while a sparing of the component at 8 Hz was always paralleled by a sparing of the same component at 32 Hz.9 These findings strongly support the idea that, at least for the human macular flicker ERG, fundamental components at both 8 and 32 Hz share common generators. In conclusion, while future experimental studies may further clarify the origin of primate macular flicker ERG, the available evidence, including that provided by the Kondo and Sieving1 paper, supports different retinal origins for the fundamental and second harmonic, as well as their use in probing the activity of distal (i.e. photoreceptors/bipolar cells) versus proximal (ganglion cells/amacrine cells) retinal layers, respectively. Benedetto Falsini Accepted for publication July 20, 2001 Corresponding author: References 1. Kondo M, Sieving PA. Primate photopic sine-wave flicker ERG: vector modeling analysis of component origins using glutamate analogs. Invest Ophthalmol Vis Sci. 2001;42:305-312. 2. Falsini B, Iarossi G, Porciatti V, et al. Postreceptoral contribution to macular dysfunction in retinitis pigmentosa. Invest Ophthalmol Vis Sci. 1994;35:4282-4290. 3. Falsini B, Iarossi G, Fadda A, et al. The fundamental and second harmonic of the photopic flicker electroretinogram: temporal frequency-dependent abnormalities in retinitis pigmentosa. Clinical Neurophysiol. 1999;110:1554-1562. 4. Porciatti V, Falsini B. Inner retina contribution to the flicker electroretinogram: a comparison with the pattern electroretinogram. Clinical Vision Sciences. 1993;8:435-437. 5. Baker CL, Hess RF, Olsen BT, Zrenner E. Current source density analysis of linear and non-linear components of the primate electroretinogram. J Physiol. 1988; 407:155-176. [Abstract] 6. Morrone C, Fiorentini A, Bisti S, Porciatti V, Burr DC. Pattern-reversal electroretinogram to chromatic stimuli: II Monkey. Vis Neurosci. 1994;11:873-884. 7. Falsini B, Colotto A, Porciatti V, et al. Macular flicker- and pattern-ERGs are differently affected in ocular hypertension and glaucoma. Clinical Vision Sciences. 1991;6:423-429. 8. Falsini B, Porciatti V, Fadda A, et al. The first and second harmonic of macular flicker electroretinogram: differential effects of retinal diseases. Doc Ophthalmol. 1995;90:157-167. 9. Porciatti V, Falsini B, Fadda A, Bolzani R. Steady-state analysis of the focal ERG to pattern and flicker: relationship between ERG components and retinal pathology. Clinical Vision Sciences. 1989;4:323-332. |
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