Variability in the Time Course of Single Photon Responses from Toad Rods Termination of Rhodopsin’s Activity

AbstractWe examined the responses of toad rod photoreceptors to single photons of light. To minimize the effects of variability in the early rising phase, we selected sets of responses that closely matched the rise of the mean single photon response. Responses selected in this way showed substantial variations in kinetics, appearing to peel off from a common time course after different delays. Following incorporation of the calcium buffer BAPTA, the time to peeling off was retarded. Our analysis indicates that it is not necessary to invoke a long series of reaction steps to explain the shutoff of rhodopsin activity. Instead, our results suggest that the observed behavior is explicable by the presently known shutoff reactions of activated rhodopsin, modulated by feedback

Multiple Steps of Phosphorylation of Activated Rhodopsin Can Account for the Reproducibility of Vertebrate Rod Single-photon Responses

Single-photon responses (SPRs) in vertebrate rods are considerably less variable than expected if isomerized rhodopsin (R*) inactivated in a single, memoryless step, and no other variability-reducing mechanisms were available. We present a new stochastic model, the core of which is the successive ratcheting down of R* activity, and a concomitant increase in the probability of quenching of R* by arrestin (Arr), with each phosphorylation of R* (Gibson, S.K., J.H. Parkes, and P.A. Liebman. 2000. Biochemistry. 39:5738–5749.). We evaluated the model by means of Monte-Carlo simulations of dim-flash responses, and compared the response statistics derived from them with those obtained from empirical dim-flash data (Whitlock, G.G., and T.D. Lamb. 1999. Neuron. 23:337–351.). The model accounts for four quantitative measures of SPR reproducibility. It also reproduces qualitative features of rod responses obtained with altered nucleotide levels, and thus contradicts the conclusion that such responses imply that phosphorylation cannot dominate R* inactivation (Rieke, F., and D.A. Baylor. 1998a. Biophys. J. 75:1836–1857; Field, G.D., and F. Rieke. 2002. Neuron. 35:733–747.). Moreover, the model is able to reproduce the salient qualitative features of SPRs obtained from mouse rods that had been genetically modified with specific pathways of R* inactivation or Ca(2+) feedback disabled. We present a theoretical analysis showing that the variability of the area under the SPR estimates the variability of integrated R* activity, and can provide a valid gauge of the number of R* inactivation steps. We show that there is a heretofore unappreciated tradeoff between variability of SPR amplitude and SPR duration that depends critically on the kinetics of inactivation of R* relative to the net kinetics of the downstream reactions in the cascade. Because of this dependence, neither the variability of SPR amplitude nor duration provides a reliable estimate of the underlying variability of integrated R* activity, and cannot be used to estimate the minimum number of R* inactivation steps. We conclude that multiple phosphorylation-dependent decrements in R* activity (with Arr-quench) can confer the observed reproducibility of rod SPRs; there is no compelling need to invoke a long series of non-phosphorylation dependent state changes in R* (as in Rieke, F., and D.A. Baylor. 1998a. Biophys. J. 75:1836–1857; Field, G.D., and F. Rieke. 2002. Neuron. 35:733–747.). Our analyses, plus data and modeling of others (Rieke, F., and D.A. Baylor. 1998a. Biophys. J. 75:1836–1857; Field, G.D., and F. Rieke. 2002. Neuron. 35:733–747.), also argue strongly against either feedback (including Ca(2+)-feedback) or depletion of any molecular species downstream to R* as the dominant cause of SPR reproducibility

Analogue Models for T and CPT Violation in Neutral-Meson Oscillations

Analogue models for CP violation in neutral-meson systems are studied in a general framework. No-go results are obtained for models in classical mechanics that are nondissipative or that involve one-dimensional oscillators. A complete emulation is shown to be possible for a two-dimensional oscillator with rheonomic constraints, and an explicit example with spontaneous T and CPT violation is presented. The results have implications for analogue models with electrical circuits.Comment: 9 page

Parameters of the Magnetic Flux inside Coronal Holes

Parameters of magnetic flux distribution inside low-latitude coronal holes (CHs) were analyzed. A statistical study of 44 CHs based on Solar and Heliospheric Observatory (SOHO)/MDI full disk magnetograms and SOHO/EIT 284\AA images showed that the density of the net magnetic flux, $B_{{\rm net}}$, does not correlate with the associated solar wind speeds, $V_x$. Both the area and net flux of CHs correlate with the solar wind speed and the corresponding spatial Pearson correlation coefficients are 0.75 and 0.71, respectively. A possible explanation for the low correlation between $B_{{\rm net}}$ and $V_x$ is proposed. The observed non-correlation might be rooted in the structural complexity of the magnetic field. As a measure of complexity of the magnetic field, the filling factor, $f(r)$, was calculated as a function of spatial scales. In CHs, $f(r)$ was found to be nearly constant at scales above 2 Mm, which indicates a monofractal structural organization and smooth temporal evolution. The magnitude of the filling factor is 0.04 from the Hinode SOT/SP data and 0.07 from the MDI/HR data. The Hinode data show that at scales smaller than 2 Mm, the filling factor decreases rapidly, which means a mutlifractal structure and highly intermittent, burst-like energy release regime. The absence of necessary complexity in CH magnetic fields at scales above 2 Mm seems to be the most plausible reason why the net magnetic flux density does not seem to be related to the solar wind speed: the energy release dynamics, needed for solar wind acceleration, appears to occur at small scales below 1 Mm.Comment: 6 figures, approximately 23 pages. Accepted in Solar Physic