Abstract
The action of acetylcholine (AC) on the melanophores was tested by Parker 1 , 2 on the Fundulus and Ameiurus. When he found in 1931 that AC, unprotected by physostigmine, caused dispersion of the melanophore pigment in fairly large dose, he concluded that AC does not play a part in its normal control. And when he found in 1934 that AC, protected by physostigmine, caused a slight concentration of the melanophore pigment in fairly large amount, he made the same conclusion. Recent experiments done on the paradise fish (Macropodus opercularis) suggested, however, that AC may be involved in the mechanism of melanophore expansion in this species.
It was consistently demonstrated that 0.01γ AC chloride (E. Merck) injected into the body subcutaneously could produce a local black area of 8×8 sq mm within 30–45 sec. after the injection, lasting for 10–13 min. Under binocular microscope, the melanophores were found to be expanded.
A purified extract was made from the caudal fins according to the method of Chang, Hsieh, Lee, Li and Lim 3 and was tested on toad's rectus and heart, and leech, (Whitmania acranulata, Whitman). AC was identified by the ratio between the unknown and the AC-standard before and after eserine on the rectus (Chang and Gaddum 4 ), the atropine test on the heart, and the acid-alkali test on the leech. The extract was found to contain 0.5–1.0γ AC (as chloride) per g wet tissue.
Injection of an extract equivalent to 0.009γ AC could produce blackness in the caudal fin comparable to that produced by an equal amount of the AC-standard.
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