Antagonistic Process as Source of Visible-Light Suppression of Afterpotential in Limulus UV Photoreceptors

[Brief letters to the Editor that make specific scientific reference to papers published previously in THE JOURNAL OF GENERAL PHYSIOLOGY are invited. Receipt of such letters will be acknowledged, and those containing pertinent scientific comments and scientific criticisms will be published.] Antagonistic Process as Source of Visible-Light Suppression of Afterpotential in Limulus UV Photoreceptors Dear Sir: The relation between the visual pigment cascade and the membrane potential changes which result from the absorption of photons in photoreceptors is still unclear. Nolte and Brown (1), working on the UV cells of the median eye of Limulus, have recently established an interesting correlation between the induction and suppression by light of a prolonged depolarizing afterpotential (PDA) and the hypothetical photoconversion of the visual pigment from the primary state (VP360) to a metastable photoproduct (M480) and the reverse photoconversion, respectively. However, they offered a tentative model relating the depolarization directly to the presence of M480 or dark conversion of M480 into VP360. We present evidence suggesting that (a) no pigment change takes place during the dark decline of the PDA, and (b) the pigment does not return in the dark to its original state at least for hours at room temperature. (We assume, as do Nolte and Brown, that this cell contains only one visual pigment. No cells are known to contain more than one.) The observations (1, 2) on which Nolte and Brown based their model relate to the very slow repolarization in the dark of a UV cell depolarized by strong UV stimulation (see trace A of Fig. 1). This PDA can be rapidly suppressed by visible light (as in trace D of Fig. 1). The model suggests that the dark decay and the suppression by light of the PDA are due to the return of the pigment to the VP360 state, by slow conversion in the dark, or by photoregeneration. If the dark decay of the PDA were directly linked to the return of the pigment to its primary state, however, one would expect that further UV stimulation of a cell in which a maximal PDA has declined to base line would again induce a PDA. This turns out not to be the case. Trace A of Fig. 1 (see reference 3 for Methods) shows the intracellular response to UV light (360 nm) of a cell which had been exposed 5 min earlier to strong visible light (550 nm), and …