Presynaptic nicotinic potentiation of a frog retinotectal transmission evoked by discharge of a single retina ganglion cell

It was demonstrated in our previous studies of the frog retinotectal transmission that retinotectal synaptic potentials are enhanced by a factor of 1.5 due to the tonic presynaptic nicotinic potentiation, caused by the ambient level of the acetylcholine in the frog tectum. Furthermore, the results of those studies have indicated that the mechanism of the nicotinic potentiation is only partially exploited, because the application of the cholinergic agonist had increased the retinotectal transmission more than 2 times above the level of the tonic potentiation. The purpose of the present study was to explore this additional potentiation. We have shown that: (1) Bursts of 4–10 action potentials of a frog retina ganglion cell gave rise to an increase (phasic potentiation) of the retinotectal transmission 1.4–2.2 times, depending on the burst strength, that lasted tens of seconds. (2) This increase has been mediated through the presynaptic nicotinic acetylcholine receptors activated by the endogenous acetylcholine released into the tectum during relatively strong bursts of the retina ganglion cell. (3) Two types of the nicotinic acetylcholine receptors are co-localized in the presynaptic terminals of the individual retinotectal input to the tectum layer F – high-affinity (tonic) and low-affinity (phasic) nicotinic receptors.

► We investigated the burst-induced facilitation of a frog retinotectal transmission.
► A substantial (∼2 times) increase of the retinotectal transmission was demonstrated.
► This increase depended on the preceding burst strength and lasted ∼30 s.
► The increase was mediated by the presynaptic nicotinic receptors.
► These receptors exhibited a relatively low-affinity to the agonist acetylcholine.