The cellular origin of the b-wave in the electroretinogram? a developmental approach

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Abstract
Retinal ganglion cells and retinotectal synapses of chick embryos can be activated by electrical stimulation at early stages of development (Rager, '76a,b), whereas light evoked responses occur only towards the end of the incubation period. Thus, photoreceptors seem to be the last cells to mature in the chain of elements necessary to enable transmission of visual information to tectal neurons. In the present study the development of light evoked activity in the retina was investigated and compared with the strutural maturation of retinal cells. This ontogenetic approach offers a solution to the problem of the cellular origin of the b‐wave called in question by recent records of the potassioretinogram (KRG). Lamellar structures in the developing outer segments of photoreceptors can first be observed on incubation day 17. Late on the same day a corneal electroretinogram (ERG) and a visual evoked response on the optic tectum (VER) can be recorded. The response properties of the developing b‐wave and VER were tested using various stimulus parameters. From the latencies of the b‐wave and of the VER it is concluded that the b‐wave is not generated directly by the activity of neurons involved in intraretinal signal transmission. Thus it is necessary to consider secondary processes triggered by neuronal activity such as depolarization of glial cells. In the chick retina, Müller cells are virtually the only glial cells. They fulfill all structural requirements necessary to explain the current which spreads through the retina during the b‐wave. Electronmicroscopic analysis reveals that Müller cells undergo drastic changes during the early phase of b‐wave development (incubation day 18). In particular, the number of microtubules per unit volume and the surface area of Müller cell processes in the outer plexiform layer increase considerably. It is, therefore, suggested that the b‐wave originates in the depolarization of Müller cells secondary to synaptic activity in the outer plexiform layer.