The purpose of this study was to evaluate the use of slow multifocal m-sequence stimulation in analyzing the topographic distribution and underlying mechanisms (including nonlinearities) of the retinal oscillatory potentials (OPs). In giving us access to the response topography and the nonlinear characteristics of the OP,, the m-sequence technique provides us with two important means for the identification and characterization of the signal sources. In this study, we analyzed the OPs into the first- and second-order components and investigated their topographies and luminance dependence. The distribution of both the first- and second-order OP components differed significantly from that of the nicker ERG investigated by Sutter and Tran (1992). At eccentricities and luminance levels favoring activity by both rods and cones, the second-order OPs were particularly prominent showing the most clear-defined and complex waveform The topographic distribution of the second-order OPs showed combined features of both rod and cone distributions On a strong rod-bleaching background the second-order OPs were eliminated and the first-order OPs showed a reduced amplitude and a shifted latency These results are consistent with the notion that the second-order component of the OPs is dominated by contributions from rod-cone interactions.

We found that a single intravitreal injection of 6-hydroxy dopamine (6-OHDA) is highly efficient in blocking the development of deprivation-induced myopia in young chickens. To investigate the effects of 6-OHDA on retinal function, we studied electroretinograms (ERGs) in chickens aged 15-25 days, 4 days subsequent to the injection. Both spectral sensitivity and oscillatory potentials were tested. In addition, a histological examination was performed of dopaminergic amacrine cells labeled by a monoclonal antibody against tyrosine hydroxylase. We found that, at doses of 6-OHDA sufficient to suppress deprivation myopia entirely, no effect could be detected on either the ERGs or on the density and appearance of dopaminergic amacrine cells. For higher doses, spectral sensitivity and the number of dopaminergic amacrine cells declined gradually. In contrast, as doses increased, oscillatory potentials 1 and 2 grew in amplitude only to decline at the highest doses. The results indicate that (1) development of deprivation myopia requires normal retinal function and that (2) slight changes in the gains of dopaminergic pathways are sufficient to block the development of deprivation myopia.

Most of the blinding retinopathies are due to progressive photoreceptor degeneration. Treatment paradigms that are currently being investigated include strategies to either halt or slow down photoreceptor cell loss, or to replace useful vision with retinal prosthesis. However, more information is required on the pathophysiological changes of the diseased retina, in particular the inner retina, that occur as a consequence of photoreceptor cell loss. Here we wished to use light damage as a stoppable insult to determine the structural and functional consequences on inner and outer retina, with the overall goal of determining whether survival of a functional inner retina is possible even if the outer retina is damaged. Mice were exposed to a 20-day light-damage period. Electroretinograms (ERG) and morphology were used to assess subsequent recovery. Outer retina was monitored analyzing a-waves, which represent photoreceptor cell responses, and histology. Integrity of the inner retina was monitored, analyzing b-waves and oscillatory potentials (OP1–OP4) and immunohistochemical markers for known proteins of the inner retina. All six ERG components were significantly suppressed with respect to amplitudes and kinetics, but stabilized in a wave-dependent manner within 40–70 days after the end of light exposure. As expected, damage of the outer retina was permanent. However, function of the inner retina was found to recover significantly. While b-wave amplitudes remained suppressed to 60% of their baseline values, OP amplitudes recovered completely, and implicit times of all components of the inner retina (b-wave and OP1–OP4) recovered to a level close to baseline values. Histological analyses confirmed the lack of permanent damage to the inner retina. In summary, these data suggests that the inner retina has the potential for significant recovery as well as plasticity if treatment is available to stop the deterioration of the outer retina.

The separate components of the dark-adapted electroretinogram (ERG) are believed to reflect the electric activity of neurones in both the inner and the outer layers of the retina, although their precise origin still remains unclear. The purpose of this study was to examine whether selective blockage or stimulation of the different subtypes of GABA receptors might help further elucidate the cellular origin of the components of the dark-adapted ERG. The rat retina is of interest since the localization and physiology of GABA receptors in that retina have been examined in great detail. GABA agonists and antagonists, known to affect the responses of neurons in the inner plexiform layer, were injected into the vitreous of one eye while ERG responses evoked by flashes of white light were recorded. GABA and the GABAa agonist isoguvacine completely removed the oscillatory potentials (OPs) and reduced the amplitude of the a- and b-waves. TPMPA, a GABAc antagonist, reduced the a- and b-waves but had no significant effect on the OPs. Baclofen, a GABAb agonist, reduced the amplitude of the a- and b-waves, without having any effects on the amplitude of the OPs. The GABAb antagonist CGP35348 increased the amplitudes of the a- and b-wave without having an effect on the amplitudes of the OPs. The GABAb receptor ligands had significant and opposite effect on the latency of the OPs. These results indicate that retinal neurons, presumably a subpopulation of amacrine cells, that have GABAb receptors are not the source of the OPs of the ERG, although they may modulate these wavelets in some manner, while contributing to the generation of the dark-adapted a- and b-waves. OPs are modified by stimulation of GABAa receptors, and the a- and b-waves by stimulation of all GABA receptor subtypes.

Retinal neurons are generated in overlapping growth spurts with ganglion cell and cone populations peaking sooner than rod and bipolar cell numbers. As such the functional development of the inner and outer retinal components and elements within these strata (rods vs. cones) may differ. We considered the postnatal development of the postreceptoral components of the ERG (P2, oscillatory potentials) in the guinea pig. ERGs were also evaluated across albino and pigmented strains in order to consider the role that pigmentation has for functional development. Electroretinograms were collected on postnatal days PD1 to PD60 (n = 4–7 per time point). The postreceptoral P2 amplitude and implicit time was extracted (digital subtraction of modelled P3 and filtering, 0.5–49 Hz). Intensity–response relationships were described using Naka–Rushton functions whose parameters were compared using a nonparametric bootstrap. Oscillatory potentials (OPs) were extracted following signal conditioning and filtering to remove the a- and b-waves and were described using a Gabor function. OP response parameters were compared using repeated measures ANOVA. Postreceptoral P2 amplitudes mature soon after birth (PD10–PD12). Oscillatory potentials show a similar postnatal amplitude development (PD10–PD12) but a later maturation in timing (PD20) compared with the postreceptoral waveform. All components (P3, P2, and OPs) declined at the same relative rate with age after PD12. Albino animals gave larger, faster, and more sensitive waveforms at all ages but showed the same age-related trends as did pigmented animals. Early development of inner retinal synapses in guinea pigs may underlie the rapid postnatal maturation of their postreceptoral response. These appear to be constrained by the development of receptoral responses. All components declined at the same rate suggesting either a change in the photoreceptoral response or changes to ocular impedance with age.