title: Do pyrethroids activate neurotransmitter receptors?
abstract: 1. Leech Retzius (R) neurons are excited by carbachol, and this action is blocked by benzoquinonium (Mytolon). 2. Pyrethroids induce spontaneous depolarizations in R neurons. These events are not blocked by benzoquinomium, therefore pyrethroids are not acting on the cholinoreceptor. 3. A congeneric series of synthetic pyrethroids, the QSAR compounds, also induce depolarizations in R cells. The log time to onset of these events is correlated with polarity of the molecule and the structure of the acid moiety, the dichlorovinyl esters being more effective neurotoxicologically than the corresponding chrysanthemates. 4. The depolarizations induced by pyrethroids are not blocked by tetrodotoxin (TTX) in either pressure-sensitive (P) or nociceptive (N) neurons, in which the spike is TTX-sensitive, or in R neurons which have an action potential resistant to TTX. The depolarizations are thus not due to ionic currents moving in through fast sodium channels.
mesh_terms: D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D066298:In Vitro Techniques; D007865:Leeches; D008564:Membrane Potentials / Q000187:drug effects; D011722:Pyrethrins / Q000494:pharmacology*; D000644:Quaternary Ammonium Compounds / Q000494:pharmacology; D017981:Receptors, Neurotransmitter / Q000187:drug effects*; D013779:Tetrodotoxin / Q000494:pharmacology
chemical_list: D011722:Pyrethrins; D000644:Quaternary Ammonium Compounds; D017981:Receptors, Neurotransmitter; D013779:Tetrodotoxin; D002217:Carbachol; C004991:benzoquinonium