Abstract
The effects on the oscillatory potentials (OP) of the ERG [electroretinogram] of some pharmacological agents, which antagonize the putative neurotransmitters glutamate aspartate and dopamine were tested in the mudpuppy. GDEE [L-glutamic acid diethyl ester] and .alpha.-aminoadipate, blocking agents of the excitatory amino acids glutamate and aspartate, respectively, decreased the amplitude of all the OP. The amplitude of the b-wave was simultaneously reduced. No selective or differential sensitivity of the OP was found, which suggests that glutamate- or aspartate-sensitive neuronal pathways do not seem to be directly involved in the generation of the OP. Haloperidol, which antagonizes the effect of the inhibitory transmitter agent dopamine, differentially affected the OP. The earlier OP 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. The individual oscillatory peaks are likely to have different origins and only inhibitory feed-back synapses give rise to the OP.