Effect of nicotine and acetylcholine on crustacean muscle membrane potential.
We have investigated the effect of nicotine and acetylcholine on the resting membrane potential of the crayfish extensor muscle in order to determine whether crustacean muscle can be activated by cholinergic compounds. Intracellular recordings from individual deep extensor abdominal muscle cells were made using standard glass microelectrode techniques. The resting membrane potential was measured before and after treatment with glutamate, nicotine, and acetylcholine. Glutamate, which is a known activator of crayfish muscle, was used to determine whether the muscle cell preparation was viable and capable of responding to any of the test substances. Our results confirm that application of glutamate is associated with a depolarization of the muscle membrane. However, muscle cells showed no depolarization after treatment with nicotine (50 microM) or acetylcholine (66 microM). These results argue against the notion that increases in muscle tension may be responsible for the increased receptor organ discharge observed in the presence of nicotine. Rather, it supports the hypothesis that nicotine is acting directly on the mechanoreceptor membrane to change its sensitivity.
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D003400:Astacoidea / Q000502:physiology*; D005971:Glutamates / Q000494:pharmacology; D018698:Glutamic Acid; D008564:Membrane Potentials / Q000187:drug effects; D009132:Muscles / Q000187:drug effects*; D009538:Nicotine / Q000494:pharmacology*
D005971:Glutamates; D018698:Glutamic Acid; D009538:Nicotine; D000109:Acetylcholine