EOG and ERG modifications induced in the chicken eye after blockade of catecholamine and 5-hydroxytryptamine biosynthesis

Abstract

The involvement of catecholaminergic and indoleaminergic systems in the modulation of the standing potential of the eye was tested in chickens by means of an indirect electrooculography method and direct current electroretinogram recordings. D,L alpha-monofluoromethyl dopa (MFMD), 50 and 100 nmol), a highly specific inactivator of aromatic L-amino acid decarboxylase, was injected intravitreally. This treatment is known to induce a selective and irreversible blockade of dopamine and 5-hydroxytryptamine biosynthesis. Five hours after drug injection an important increase in the standing potential appeared. The light peak was delayed by about 5 min but its amplitude was unchanged. The return of the standing potential to basal value during maintained illumination was delayed by 5-10 min. The time course of the dark trough was not modified. The intensity-voltage functions were also studied for the various electroretinogram components, 5 hr after MFMD. The voltage of the b-wave was reduced (by 65% with the highest intensity), while the other components were little affected. Substantial reduction in dopamine and 5-hydroxytryptamine concentrations were found in treated retinas. These data, together with previous results, suggest that the standing potential of the chicken eye may be modulated by a balance between catecholamine and indoleamine systems.

Electrooculographic and electroretinographic study in the chicken after dopamine and haloperidol

“…These data lead to the hypothesis that dopamine, which is present in amacrine and/or interplexiform cells in various species [3] and released by light [4], or another molecule related to dopamine might be a modulator of the standing potential and of the light peak. Previous works using the neurotoxin 6-hydropydopamine [2] or blockers of dopamine biosynthesis [5] are in agreement with such a hypothesis. In the present work we studied the acute modifications induced on the electrooculogram (EOG) and the electroretinogram (ERG) components by blockade of dopamine D1 and D2 receptors by using the neuroleptic drug haloperidol, a nonspecific dopamine antagonist.…”