Further studies of the chemical sensitivity of the oscillatory potentials of the electroretinogram (ERG). II. Glutamate-aspartate-and dopamine antagonists.
The effects on the oscillatory potentials (OPs) of the ERG of some pharmacological agents, which antagonize the putative neurotransmitters glutamate aspartate and dopamine were tested. GDEE and alpha-aminoadipate, blocking agents of the excitatory amino acids glutamate and aspartate, respectively, decreased the amplitude of all the OPs. The amplitude of the b-wave was simultaneously reduced. Thus, no selective or differential sensitivity of the OPs was found, which suggests that glutamate- or aspartate-sensitive neuronal pathways do not seem to be directly involved in the generation of the OPs. Haloperidol, which antagonizes the effect of the inhibitory transmitter agent dopamine, differentially affected the OPs. The earlier OPs appeared more sensitive to low doses of the drug than the later ones. Such doses only slightly decreased the maximum amplitude of the b-wave and did not affect the a-wave. Thus, these findings indicate and support previous suggestions that the individual oscillatory peaks are likely to have different origins and that only inhibitory feed-back synapses give rise to the OPs.
D015074:2-Aminoadipic Acid / Q000494:pharmacology; D000818:Animals; D001224:Aspartic Acid / Q000037:antagonists & inhibitors*; D018492:Dopamine Antagonists; D004596:Electroretinography; D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates / Q000494:pharmacology; D006220:Haloperidol / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects*; D012160:Retina / Q000502:physiology*
D018492:Dopamine Antagonists; D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates; C011829:glutamic acid diethyl ester; D015074:2-Aminoadipic Acid; D001224:Aspartic Acid; D006220:Haloperidol