Abstract
Purpose: :
In the presence of a rod-saturating background field, photic stimuli of increasing intensity results in a graded increase in the amplitude of the ERG a-wave. In contrast, the b- and d- waves (On-, Off-responses, respectively) increase initially, but then decrease in response to stimuli of higher intensity. This phenomenon, first described in human ERG corneal recordings, is known as the "photopic hill" (PH) effect. The origin is unknown, and we sought to identify the neural mechanism responsible for the PH effect in the present study.
Methods: :
Vitreous-ERG recordings, from an excised tiger salamander eyecup with the cornea and lens removed, were collected and analyzed with Powerlab software (ADinstruments Inc.). Gravity perfusion, ~2.0mL/min, provided fresh Ringer solution or drug (Sigma, Tocris, Ascent) to the retinal surface. Light adaptation, prior to stimulation, for 30 minutes to 1 hour in a standard rod-saturating background (ISCEV std, ~25 cd/m^2). A Mercury burner provided a shutter-controlled white flash (~600ms), with gradually increasing luminance from 1 to 2,500 cd·s/m^2 in ascending order.
Results: :
In response to increasing stimulus intensity, the b- and d-waves of the light-adapted ERG increased at low and medium intensities, and decreased at higher intensities, thus mimicking the PH effect described in humans. The PH phenomenon was more evident in the d-wave, but it was insensitive to agents (APB, CNQX) that blocked either the ON- or OFF-pathways in the distal retina. TTX could not eliminate the PH effect, nor was it sensitive to the GABA receptor antagonist SR95531. However, blockage of glycine and GABA receptors with strychnine and SR95531 abolished the PH effect in both the b- and d-wave components of the photopic ERG.
Conclusions: :
Since strychnine could effectively eliminate the PH effect in the amphibian ERG, it appears that glycinergic feedback provides a potential neural mechanism underlying the origin of the PH phenomenon.
Keywords: electroretinography: non-clinical • inhibitory neurotransmitters • signal transduction: pharmacology/physiology