PubMed · 5678321
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H C Berg. 1968. Membrane dipole potentials.. https://doi.org/10.1016/s0006-3495(68)86538-5
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Chromatophores from Rhodobacter capsulatus were incubated in the dark with NADPH and acetylpyridineadenine dinucleotide (AcPdAD+) in the presence of different concentrations of myxothiazol. The transhydrogenase activity was monitored until an appropriate mass action ratio, [AcPdAD+][NADPH]/[AcPdADH][NADP+], was reached. The sample was then illuminated and the initial rate of either AcPdAD+ reduction by NADPH or AcPdADH oxidation by NADP+ was recorded. The ratio of H+ translocated per H- equivalent transferred by transhydrogenase was calculated from the value of the membrane potential (delta pH = 0) at which illumination caused no net reaction in either direction. The mean value for the H+/H- ratio was 0.55. At greater values of [AcPdAD+][NADPH]/[AcPdADH][NADP+] than were employed in the above experiments and over a wider range of concentrations of myxothiazol, it was found that incremental increases in the membrane potential always gave rise to a decrease, never an increase in the rate of AcPdAD+ reduction. In contrast to the H(+)-ATP synthase, there is no evidence of any activation/deactivation of H(+)-transhydrogenase by the protonmotive force.
A stochastic model for single neuron's activity is constructed as the continuous limit of a birth-and-death process in the presence of a reversal hyperpolarization potential. The resulting process is a one dimensional diffusion with linear drift and infinitesimal variance, somewhat different from that proposed by Lánský and Lánská in a previous paper. A detailed study is performed for both the discrete process and its continuous approximation. In particular, the neuronal firing time problem is discussed and the moments of the firing time are explicitly obtained. Use of a new computation method is then made to obtain the firing p.d.f. The behaviour of mean, variance and coefficient of variation of the firing time and of its p.d.f. is analysed to pinpoint the role played by the parameters of the model. A mathematical description of the return process for this neuronal diffusion model is finally provided to obtain closed form expressions for the asymptotic moments and steady state p.d.f. of the neuron's membrane potential.
The general mechanisms by which chemical stimuli may influence the firing frequency of olfactory neurons were briefly described. They include specific mechanisms mediated by receptor molecules and nonspecific mechanisms involving general properties of the chemicals and of cells. It is difficult to imagine that odorant mixtures influence receptor cells by mechanisms that are fundamentally different from those by which homogeneous chemicals act. It is argued that even under the best experimental conditions the presentation of odorants usually or always involves exposing the receptor cells to more than one additional molecular species compared to the unstimulated condition. This is because odorants invariably have contaminants that may be of potency such that their contribution to the odor is large even though their contribution to the number of molecules in the stimulus stream is small. Furthermore, the partition coefficients of the major and minor components are unlikely to be identical; therefore, their relative concentrations in the aqueous environment of the receptor cells can differ greatly from that in the gas phase. Finally, metabolic transformations of odorants in the olfactory mucosa can result in the exposure of receptor cells to mixtures of odorant and metabolites, with the mixture composition varying with time. Finally, some pitfalls in analyzing the effects of odorant mixtures are discussed. At the very least, it is necessary to determine the relation of concentration to response for each odorant in the mixture in order to interpret results in terms of interactions. Even with such data caution must be used, especially in attaching significance to reductions in the apparent maximal responses to one odorant induced by the presence of the other.