Retinal co-mediator acetylcholine evokes muscarinic inhibition of recurrent excitation in frog tectum column

• It was shown that recurrent excitatory transmission in the frog tectum column.
• Is inhibited by the endogenous acetylcholine.
• The inhibition occurs with a delay of ∼80 ms.
• Muscarinic AChR antagonist atropine eliminates this effect of endogenous ACh.
• Thus, the delayed inhibition is mediated by the activation of muscarinic AChRs.

Acetylcholine receptors contribute to the control of neuronal and neuronal network activity from insects to humans. We have investigated the action of acetylcholine receptors in the optic tectum of Rana temporaria (common frog). Our previous studies have demonstrated that acetylcholine activates presynaptic nicotinic receptors, when released into the frog optic tectum as a co-mediator during firing of a single retinal ganglion cell, and causes: a) potentiation of retinotectal synaptic transmission, and b) facilitation of transition of the tectum column to a higher level of activity. In the present study we have shown that endogenous acetylcholine also activates muscarinic receptors, leading to a delayed inhibition of recurrent excitatory synaptic transmission in the tectum column. The delay of muscarinic inhibition was evaluated to be of ∼80 ms, with an extent of inhibition of ∼2 times. The inhibition of the recurrent excitation determines transition of the tectum column back to its resting state, giving a functional sense for the inhibition.

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