Abstract
Abstract: :
Purpose: Cholinergic and GABAergic mechanisms have been demonstrated to be involved in retinal motion coding. Whether and how blockade of GABAergic and cholinergic receptors affect temporal transfer properties (TTP) was investigated under comparable experimental conditions in both the ERG and behavioral experiments. Methods: Temporal transfer properties were determined from vitreal ERG recordings under photopic conditions as well as from behavioral, two–choice forced procedure, experiments before and after injection of curare (10 microM intra–occular concentration, nicotinic ACh–R antagonist), atropine (100 microM intra–occular concentration, muscarinic ACh–R antagonist) or bicuculline (30 microM and 67 microM intra–occular concentration, GABAa–R antagonist). Results: The gain–frequency plots determined from ERG recordings and from behavioral experiments are very similar in shape (Mora–Ferrer and Behrend, in press). The ERG data can be described as a 3rd order low–pass filter with resonance having an upper limit frequency of about 30 Hz. Atropine shifts the gain–frequency characteristic to a lower limit frequency without changing its shape. Curare changes the limit frequency and the characteristic of the gain–frequency plot to that of a pure low–pass, i.e. the resonance is removed. Bicuculline removes the resonance and in addition lowers the order of the low–pass filter and the limit frequency. Post–injection of bicuculline, the gain–frequency plot generated with behavioral data has a comparable limit frequency to the ERG–data but falls off rather steeply. Conclusions: Nicotinic and GABAergic receptor mediated mechanisms appear to be involved in the generation of the resonance property of the TTP while muscarinic receptors do not seem involved. The generation of the resonance property of the TTP occurs most probably in the inner retina since actions of nicotinic ACh–receptors have been reported in the inner retina. The site of action must be a cell type visible in the ERG, i.e. not the ganglion cells. Changes of the resonance part of the TTP could occur due to either changes in inhibitory strength or an phase– shift of the inhibition. This is in line with the GABAergic control of bipolar cell output as deduced from modulatory action of dopamine (Mora–Ferrer and Behrend, in press). So far, all data indicate that the well balanced timing of glutamatergic excitation and GABAergic feedback inhibition at the bipolar cell axon terminals is critical for the high frequency end of the TTP and thus the temporal resolution ability of goldfish.
Keywords: acetylcholine • inhibitory neurotransmitters • temporal vision