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Plant Alkaloid Desensitization of Fetal Muscle‐Type Nicotinic Acetylcholine Receptors

The exposure of a developing fetus to certain plant alkaloids has the potential to inhibit fetal movement which can then result in developmental defects. The putative mechanism of movement inhibition is the desensitization of fetal muscle‐type nicotinic acetylcholine receptors (nAChR) which is affected by agonist chemical structure. In this study, we tested the hypothesis that a 1,2‐dehydropiperidine alkaloid agonist is more effective at desensitizing nAChR than a saturated analogue. Agonists were evaluated in TE‐671 cells which express fetal muscle‐type nAChR, and SHSY‐5Y cells which express autonomic‐type nAChRs using a membrane potential sensing dye system. Anabaseine, a 1,2‐dehydropiperidine alkaloid, was more effective at desensitizing TE‐671 cells than anabasine which is fully saturated at the 1,2 position. The neurotransmitter acetylcholine which was included as a control was more effective than the pyridine alkaloid nicotine at desensitizing the agonist response in TE‐671 cells. Both nicotine and acetylcholine were equally effective at desensitizing the agonist response in SH‐SY5Y cells. These results suggest that anabaseine, a 1,2‐dehydropiperidine alkaloid agonist is more effective at desensitizing fetal muscle‐type nAChR than anabasine and has a greater potential to inhibit fetal movement.