Abstract
Objective: The aim of the study was to explore the effect of semi-specific antagonists and agonists of the nicotinic acetylcholine receptors on the paired-pulse facilitation and nicotinic tonic and phasic potentiation of the frog retinotectal synaptic transmission.
Materials and methods: The experiments were performed in vivo on adult frogs, Rana temporaria. An individual retina ganglion cell (or its retinotectal fiber) was stimulated by current pulses delivered through multichannel stimulating electrode positioned on the retina. Responses to a discharge of a single retinal ganglion cell were recorded in the tectum by an extracellular carbon-fiber microelectrode positioned in the terminal arborization of the retinotectal fiber in the tectum layer F. The effect of the antagonists and agonists of the nicotinic acetylcholine receptors on the tectal responses has been tested.
Results: We found that the antagonists, MLA and DHβE, and agonists, RJR-2403 and choline, of the nicotinic acetylcholine receptors of the α3β2, α4β2, α2β4, α6β2, or α7 subtypes have had no effect on the phasic and tonic potentiation of the retinotectal transmission. The pairedpulse facilitation of the retinotectal transmission was not appreciably affected by the antagonists, but the choline, agonist of the α7 subtype receptor, has significantly decreased the paired-pulse facilitation.
Conclusions: The tonic and phasic potentiation of the retinotectal transmission in the tectum layer F were not mediated by the receptors of α3β2, α4β2, α2β4, α6β2, or α7 subtype. The results suggest that presynaptic nicotinic acetylcholine receptors of the frog optic fibers are different from those of the mammalian optic fibers.
Materials and methods: The experiments were performed in vivo on adult frogs, Rana temporaria. An individual retina ganglion cell (or its retinotectal fiber) was stimulated by current pulses delivered through multichannel stimulating electrode positioned on the retina. Responses to a discharge of a single retinal ganglion cell were recorded in the tectum by an extracellular carbon-fiber microelectrode positioned in the terminal arborization of the retinotectal fiber in the tectum layer F. The effect of the antagonists and agonists of the nicotinic acetylcholine receptors on the tectal responses has been tested.
Results: We found that the antagonists, MLA and DHβE, and agonists, RJR-2403 and choline, of the nicotinic acetylcholine receptors of the α3β2, α4β2, α2β4, α6β2, or α7 subtypes have had no effect on the phasic and tonic potentiation of the retinotectal transmission. The pairedpulse facilitation of the retinotectal transmission was not appreciably affected by the antagonists, but the choline, agonist of the α7 subtype receptor, has significantly decreased the paired-pulse facilitation.
Conclusions: The tonic and phasic potentiation of the retinotectal transmission in the tectum layer F were not mediated by the receptors of α3β2, α4β2, α2β4, α6β2, or α7 subtype. The results suggest that presynaptic nicotinic acetylcholine receptors of the frog optic fibers are different from those of the mammalian optic fibers.