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Modulation of the activity of K⁺ channels by TRH and the possible involvement of this modulation in TRH-induced release of -MSH were studied in cultured frog melanotrophs, using patch-clamp and perifusion techniques. Pars intermedia cells were enzymatically dispersed and cultured in Leibovitz medium. In order to test the viability of cultured cells, the amount of -MSH released into the medium was measured by radioimmunoassay every day for 1 week of culture. The total amount of -MSH released during the first 4 days of culture was 8·6 times higher than the intracellular content of -MSH on day 1. Melanotrophs were identified by an indirect immunofluorescence technique using a specific antiserum to -MSH. Recordings obtained in whole-cell, cell-attached and excised patch-clamp configurations showed that TRH induced a transient polarization concomitant with an increase in the probability of opening of Ca²⁺-activated K⁺ channels. This transient response was followed by a depolarization accompanied by an enhanced frequency of action potential discharge. TRH also induced a decrease in voltage-dependent K⁺ conductance. Application of tetraethylammonium, a K⁺ channel blocker, depolarized the cells and increased the basal secretory level without noticeable changes in TRH-evoked -MSH release.

These results demonstrate that the neuropeptide TRH both stimulates Ca²⁺-sensitive K⁺ channels and inhibits voltage-dependent K⁺ current in pituitary melanotrophs. Our data indicate that TRH-induced secretion of -MSH is not a direct consequence of the lowering of K⁺ conductance. It thus appears that basal and TRH-induced -MSH release occur through distinct pathways; the spontaneous release of -MSH is probably linked to membrane potential, while modulation of the electrical activity is not directly involved in TRH-induced activation of the secretory process.

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