Atypical Acetylcholine Receptors on the Neurons of the Turkish Snail

by Selleckchem | Nov 17 2023

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. Induced depolarization was also suppressed by α-conotoxin RgIA, a selective inhibitor of α9 nAChR. In contrast to Lymnaea stagnalis nAChR, which are weakly sensitive to neurotoxin II and α-conotoxin GI, antagonists of muscle-type nAChR, H. lucorum receptors were most effectively inhibited by these antagonists. The results obtained, as well as the previously found sensitivity of the receptors studied in this work to muscarinic receptor ligands, indicate an unusual atypical pharmacological profile of H. lucorum nAChR.

Comments:

The study you've described investigates the effects of various nicotinic acetylcholine receptor (nAChR) ligands on acetylcholine-induced depolarization in the neurons of Helix lucorum snails. Here's a breakdown of the findings:

1. **α-Conotoxin PnIA [R9, L10]:** This is a selective antagonist of the α7 subtype of nAChR. The study found that it suppressed neuronal depolarization, suggesting that α7 nAChRs are involved in mediating acetylcholine-induced depolarization in Helix lucorum snail neurons.

2. **α-Cobratoxin:** This compound is an antagonist of both α7 and muscle-type nAChRs. It also suppressed neuronal depolarization. This indicates that both α7 and muscle-type nAChRs play a role in mediating the response to acetylcholine in these neurons.

3. **Fluorescently labeled α-bungarotoxin:** This compound is used to stain nAChRs. The study showed that the staining of neurons with fluorescently labeled α-bungarotoxin was reduced when pretreated with α-cobratoxin. This suggests that α-cobratoxin interferes with the binding of α-bungarotoxin to nAChRs, further supporting the involvement of nAChRs in these neurons.

4. **α-Conotoxin RgIA:** This is a selective inhibitor of α9 nAChRs. The study found that it suppressed induced depolarization, indicating that α9 nAChRs also play a role in mediating the response to acetylcholine in Helix lucorum snail neurons.

5. **Comparison to Lymnaea stagnalis nAChRs:** The study noted that Helix lucorum nAChRs were more effectively inhibited by neurotoxin II and α-conotoxin GI, which are antagonists of muscle-type nAChRs, in contrast to Lymnaea stagnalis nAChRs. This suggests that the nAChRs in Helix lucorum snail neurons have a different sensitivity profile compared to those in Lymnaea stagnalis.

6. **Sensitivity to muscarinic receptor ligands:** The study also mentioned that the receptors in Helix lucorum were sensitive to muscarinic receptor ligands. This indicates that these receptors have a broader pharmacological profile, responding to both nicotinic and muscarinic receptor ligands, which is somewhat atypical.

In summary, the study reveals that Helix lucorum snail neurons have a complex profile of nAChR subtypes involved in mediating acetylcholine-induced depolarization. It also suggests that these nAChRs have a unique pharmacological profile compared to other snail species, responding to a variety of ligands including both nicotinic and muscarinic receptor ligands.