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Background and Aims During the analysis of plant male meiocytes coming from destroyed meiocyte columns (united multicellular structures formed by male meiocytes in each anther locule), a considerable amount of information becomes unavailable. Therefore, in this study intact meiocyte columns were studied by volume microscopy in wild-type rye for the most relevant presentation of 3-D structure of rye meiocytes throughout meiosis. Methods We used two types of volume light microscopy: confocal laser scanning microscopy and non-confocal bright-field scanning microscopy combined with alcohol and aldehyde fixation, as well as serial block-face scanning electron microscopy. Key Results Unusual structures, called nuclear protuberances, were detected. At certain meiotic stages, nuclei formed protuberances that crossed the cell wall through intercellular channels and extended into the cytoplasm of neighbouring cells, while all other aspects of cell structure appeared to be normal. This phenomenon of intercellular nuclear migration (INM) was detected in most meiocytes at leptotene/zygotene. No cases of micronucleus formation or appearance of binucleated meiocytes were noticed. There were instances of direct contact between two nuclei during INM. No influence of fixation or of mechanical impact on the induction of INM was detected. Conclusions Intercellular nuclear migration in rye may be a programmed process (a normal part of rye male meiosis) or a tricky artefact that cannot be avoided in any way no matter which approach to meiocyte imaging is used. In both cases, INM seems to be an obligatory phenomenon that has previously been hidden by limitations of common microscopic techniques and by 2-D perception of plant male meiocytes. Intercellular nuclear migration cannot be ignored in any studies involving manipulations of rye anthers. [ABSTRACT FROM AUTHOR]

A dendritic spine is a very small structure (∼0.1 µm3) of a neuron that processes input timing information. Why are spines so small? Here, we provide functional reasons; the size of spines is optimal for information coding. Spines code input timing information by the probability of Ca2+ increases, which makes robust and sensitive information coding possible. We created a stochastic simulation model of input timing-dependent Ca2+ increases in a cerebellar Purkinje cell's spine. Spines used probability coding of Ca2+ increases rather than amplitude coding for input timing detection via stochastic facilitation by utilizing the small number of molecules in a spine volume, where information per volume appeared optimal. Probability coding of Ca2+ increases in a spine volume was more robust against input fluctuation and more sensitive to input numbers than amplitude coding of Ca2+ increases in a cell volume. Thus, stochasticity is a strategy by which neurons robustly and sensitively code information. [ABSTRACT FROM AUTHOR]

Spike timing-dependent synaptic plasticity (STDP) plays an important role in neural development and information processing in the brain; however, the mechanism by which spike timing information is encoded into STDP remains unclear. Here, we show that a novel allosteric kinetics of NMDA receptors (NMDARs) is required for STDP. We developed a detailed biophysical model of STDP and found that the model required spike timing-dependent distinct suppression of NMDARs by Ca2+-calmodulin. This led us to predict an allosteric kinetics of NMDARs: a slow and rapid suppression of NMDARs by Ca2+-calmodulin with prespiking→postspiking and postspiking→ prespiking, respectively. We found that the allosteric kinetics, but not the conventional kinetics, is consistent with specific features of amplitudes and peak time of NMDAR-mediated EPSPs in experiments. We found that the allosteric kinetics of NMDARs was also valid for synaptic plasticity induced by more complex spike trains in layer II/III of visual cortex. We extracted an essential synaptic learning rule by reduction of the allosteric STDP model and found that spike timing-dependent bidirectional role of postspiking in synaptic modification, which depends on the allosteric kinetics, is the essential principle in STDP. Thus, we propose a simple hypothesis of the allosteric kinetics of NMDARs that can coherently explain critical features of spike timing-dependent NMDAR-mediated EPSPs and synaptic plasticity. [ABSTRACT FROM AUTHOR]

Spike timing-dependent synaptic plasticity (STDP) develops neural circuits through close interaction with the firing function of single neurons. Here, we investigate the neuronal firing function dependency of STDP about a single-compartment Hodgkin–Huxley (HH) model neuron and a leaky integrate-and-fire (LIF) model neuron. Computer simulation shows that the development of synaptic strength by synaptic input pairs with constant intervals depends on the firing function of the models. The more organized packet inputs also develop synaptic strength in a firing function-dependent manner, to realize specific information processing. These results suggest that in real biological systems too, STDP with the same time window will develop different neural circuits, depending on the neuronal firing functions. © 2006 Wiley Periodicals, Inc. Syst Comp Jpn, 38(1): 41–50, 2007; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/scj.20234 [ABSTRACT FROM AUTHOR]

Sustained contraction of cells depends on sustained Rho-associated kinase (Rho-kinase) activation. We developed a computational model of the Rho-kinase pathway to understand the systems characteristics. Thrombin-dependent in vivo transient responses of Rho activation and Ca2+ increase could be reproduced in silico. Low and high thrombin stimulation induced transient and sustained phosphorylation, respectively, of myosin light chain (MLC) and myosin phosphatase targeting subunit 1 (MYPT1) in vivo. The transient phosphorylation of MLC and MYPT1 could be reproduced in silico, but their sustained phosphorylation could not. This discrepancy between in vivo and in silico in the sustained responses downstream of Rho-kinase indicates that a missing pathway(s) may be responsible for the sustained Rho-kinase activation. We found, experimentally, that the sustained phosphorylation of MLC and MYPT1 exhibit all-or-none responses. Bromoenol lactone, a specific inhibitor of Ca2+-independent phospholipase A2 (iPLA2), inhibited sustained phosphorylation of MLC and MYPT1, which indicates that sustained Rho-kinase activation requires iPLA2 activity. Thus, the systems analysis of the Rho-kinase pathway identified a novel iPLA2-dependent mechanism of the sustained Rho-kinase activation, which exhibits an all-or-none response. [ABSTRACT FROM AUTHOR]