Later, Thomas et al ., ( 1993 ) through his work with chicken ?4?2 nAChR subunits expressed on mouse M 10 cells and chicken ?7 nAChR expressed in oocytes from Xenopus laevis, showed that anatoxin-a is also a potent agonist of neuronal nAChR.
32.
This is because ( + ) anatoxin-a, the s-" cis " enone conformation, has a distance a 6.0 ?between its nitrogen and carbonyl group, which corresponds well to the 5.9 ?distance that separate the nitrogen and oxygen in acetylcholine.
33.
Electrophysiological experiments done by Spivak et al . ( 1980 ) on frogs showed that anatoxin-a is a potent agonist of the muscle-type ?12??? nAChR . Anatoxin-a induced depolarizing neuromuscular blockade, contracture of the frog's rectus abdominis muscle, depolarization of the frog sartorius muscle, desensitization, and alteration of the action potential.
34.
Electrophysiological experiments done by Spivak et al . ( 1980 ) on frogs showed that anatoxin-a is a potent agonist of the muscle-type ?12??? nAChR . Anatoxin-a induced depolarizing neuromuscular blockade, contracture of the frog's rectus abdominis muscle, depolarization of the frog sartorius muscle, desensitization, and alteration of the action potential.
35.
They compared the effects of sterilized and non-sterilized sediments on anatoxin-a degradation over the course of 22 days, and found that after that time vials with the sterilized sediments showed similar levels of anatoxin-a as at the commencement of the experiment, while vials with non-sterilized sediment showed a 25-48 % decrease.
36.
They compared the effects of sterilized and non-sterilized sediments on anatoxin-a degradation over the course of 22 days, and found that after that time vials with the sterilized sediments showed similar levels of anatoxin-a as at the commencement of the experiment, while vials with non-sterilized sediment showed a 25-48 % decrease.
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