Introduction

The electrical response of the eye to a flash of light that can be recorded at the cornea is generated by radial currents that arise either directly from retinal neurons or as a result of the effect on retinal glia of changes in extracellular potassium concentration ([K⁺]_o) brought about by the activity of these neurons. This response, the electroretinogram (ERG) (figure 12.1), is an excellent tool for studying retinal function in both the clinic and the laboratory because it can be recorded easily and noninvasively with a corneal electrode in intact subjects under physiological or nearly physiological (anesthetized) conditions. However, it is a gross potential that reflects the activity of all of the cells in the retina. For the ERG to be an effective tool in assessing normal and pathological retinal activity, it is important that the contributions of the various retinal cells be well characterized.

Figure 12.1.  

Dark- and light-adapted flash ERGs of human subjects and macaque monkeys. Top, Dark-adapted (scotopic) ERGs in response to brief high-energy flashes from darkness occurring at time zero for a normal human subject (left) and a macaque monkey (right). The stimulus energy was ∼400 sc td.s. (Source: Adapted from Robson JG, Frishman LJ.¹⁹³ Used by permission.) Bottom, Light-adapted (photopic) flash ERGs in response to longer-duration flashes on a rod-saturating background for a normal human subject (left) and a macaque monkey (right). For the human subject, the stimulus were 150 ms white ganzfeld flashes of 4.0 logphtd presented on a steady background of 3.3 log sc td. For the macaque, the same stimulus was used, but the flashes were 200 ms. (Source: Adapted from Sieving PA, Murayama K, Naarendorp F.²⁰⁹ Used by permission.)

This chapter will survey the current state of knowledge regarding the origins of better-known and more recently described waves of the ERG. There is an increasing literature on the origins of ERG in a primate model (macaque monkey) whose retina is very similar to that of humans (see figure 12.1), so work in primates will be highlighted wherever possible. Current and previous work based on other mammalian species and lower vertebrates that is critical to an understanding of the origins of the ERG will also be included. In some cases, new information based on genetically manipulated murine models will be described as well.