Restoration of the nicotinic receptor-channel activity from the blockade by atropine in bullfrog sympathetic ganglia.
Atropine (3 microM) reduced both the nicotinic and muscarinic acetylcholine (ACh) potentials of the bullfrog sympathetic ganglion cell. However, the former was completely restored within 1 h during a sustained exposure to atropine, while the latter remained blocked. Similar restorations were observed for the depressant effects on both the amplitude and decay phase of a nerve-induced postsynaptic current. The results suggest that the sustained or repetitive binding of atropine to this site results in a new conformational state capable of passing ions almost normally, but resistant to the blockade by atropine.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology*; D005071:Evoked Potentials / Q000187:drug effects; D005728:Ganglia, Sympathetic / Q000187:drug effects / Q000502:physiology*; D007473:Ion Channels / Q000187:drug effects*; D011892:Rana catesbeiana; D011976:Receptors, Muscarinic / Q000187:drug effects / Q000502:physiology; D011978:Receptors, Nicotinic / Q000187:drug effects / Q000502:physiology*
D007473:Ion Channels; D011976:Receptors, Muscarinic; D011978:Receptors, Nicotinic; D001285:Atropine; D000109:Acetylcholine