THE EFFECTS OF DRUGS AND IONS ON MELANOPHORE PIGMENT MOVEMENTS AND TRANSMEMBRANE POTENTIALS OF STONELOACH (NOEMACHEILUS)

KCl solution produced aggregation of the melanophore pigment in split fin preparations from the stoneloach (Noemacheilus barbatulus L.) which could be reversed when the solution was replaced by Young''s Ringer solution. The pigment became progressively more aggregated as the K+ concentration increased. This aggregation could be blocked by yohimbine and bretylium. It may be mediated through the release of transmitter from nerve endings. Tetrodotoxin [TTX] had no effect on the aggregation response to adrenaline [epinephrine, NE] or on the dispersion response to yohimbine, suggesting that TTX-sensitive Na channels are not involved in the movement of pigment granules. Removal of Ca2+ from the solution by EGTA [ethylene glycol bis-(.beta.-aminoethyl ether)-N,N,N'',N''-tetraacetic acid] abolished the aggregation response to KCl and inhibited the aggregation response to NE and the dispersion response to yohimbine. Substitution of acetate ions for Cl- in Young''s Ringer solution had no effect on the aggregation response to NE or the dispersion response to a subsequent application of an NE-free Ringer solution. Adrenaline bitartrate produced a uniform rapid aggregation at high concentrations. A more variable response was obtained at lower concentrations. Yohimbine hydrochloride and atropine sulfate both produced dispersion. Acetylcholine appears to play no part in pigment dispersion. Melanophore potential records showd an electrophoretic gradient from the centrosphere to the periphery along the processes of the melanophore. The sum of the centrosphere and periphery potentials remained nearly constant, although the potentials themselves varied with the position of the pigment. Application of the Nernst equation to changes in the external K+ concentration produced a regression line with a slope of 47 and its intercept predicted an intracellular K+ concentration of 242 mmol/l. When the aggregation of the pigment also produced was blocked by yohimbine the slope of the regression line was 59 and the predicted intracellular K concentration 165 mmol/l. Na+ also contributed to the transmembrane potential. Increasing extracellular Ca produced hyperpolarization while decreasing it produced depolarization. The effects of substituting various ions for Ca2+ were also tested. Substitution of sulphate for Cl- produced a depolarization of the centrosphere potential. The use of acetate for substitution produced no such depolarization. Ouabain produced depolarization of the centrosphere and aggregation of melanophore pigment. Ouabain also inhibited the dispersion response to yohimbine. Colchicine and vinblastine both produced a slight depolarization of the cell centrosphere of dispersed cells, although the potential at the periphery appeared unaffected. Cells aggregated in KCl or adrenaline bitartrate were unable to maintain their aggregation in the presence of colchicine. Colchicine also inhibited the aggregation response to adrenaline and promoted the redispersion response to the subsequent application of adrenaline-free Young''s Ringer solution.