Atypical Acetylcholine Receptors on the Neurons of the Turkish Snail.

Using electrophysiology, the effect of nicotinic acetylcholine receptor (nAChR) ligands on acetylcholine-induced depolarization in the neurons of Helix lucorum snail was studied. It was found that the α-conotoxin PnIA [R9, L10], a selective antagonist of α7 nAChR, and α-cobratoxin (antagonist of α7 and muscle-type nAChR) suppressed neuronal depolarization. Fluorescence microscopy showed staining of the neurons with fluorescently labeled α-bungarotoxin; this staining was reduced by pretreatment with α-cobratoxin.

[Spontaneous EPSPs in Command Helix Lucorum Neurons during Geterosynaptic Potentiation].

To develop the presynaptic mechanism of the short-term plasticity of synaptic transmission the influence of the rhythmical orthodromic stimulation of intestinal nerve on the spontaneous excitatory postsynaptic potentials (EPSPs) have been analyzed in the command neurons of the defensive behavior of land snail Helix lucorum. It was shown early that the tetanic stimulation induced the short-term potentiation of evoked EPSPs. The rhythmical stimulation did not influence the amplitude of spontaneous EPSPs, but considerably increased their number.

Heterosynaptic potentiation of cholinergic excitatory postsynaptic responses of command neurons in the common snail.

Short-term heterosynaptic potentiation of cholinergic excitatory postsynaptic currents and potentials in defensive behavior command neurons was found to be evoked by stimulation of the visceral sac in the common snail. It is suggested that a mechanism increasing the choline resistance of the postsynaptic zones of command neuron membranes is involved in potentiating the excitatory postsynaptic responses to sensory stimulation.

[Heterosynaptic potentiation of cholinergic excitatory postsynaptic responses in the Helix command neurons].

Heterosynaptic potentiation of cholinergic excitatory postsynaptic currents and potentials evoked by electrical stimulation of visceral mass was discovered in command Helix neurons of escape reaction. The results suggest the involvement of mechanism of an increase in cholinosensitvity in postsynaptic membrane zones in potentiation of excitatory postsynaptic responses to sensory stimulation.

Cholinergic sensory inputs to command neurons in edible snail.

We studied cholinergic component of visceral sensory input to defensive behavior command neurons in edible snail. Nicotinic receptor antagonist tubocurarine and muscarinic receptor antagonist atropine reversibly decreased the amplitude of the total excitatory postsynaptic potential induced by electrostimulation of the peripheral region in the mechanosensory receptor field of command neurons on the surface of internal organs. Our results indicate that acetylcholine is involved in sensory signal transduction from the visceral sac to command neurons of snail parietal ganglia.