Biomedical subjects

Kazuyuki Aihara

Publications and source records attributed to Kazuyuki Aihara.

At least 19 recordsLinked to original sources

PubMed2006

Reproducing bursting interspike interval statistics of the gustatory cortex.

Cortical neurons in vivo generate highly irregular spike sequences. Recently, it was experimentally found that the local variation of interspike intervals, LV, is nearly constant for every spike sequence for the same neurons. On the contrary, the coefficient of variation, CV, varies over different spike sequences. Here, we first show that these characteristic features are also applicable in bursting spike sequences that are obtained from the rat gustatory cortex. Next, we show that the conventional leaky integrate-and-fire model does not fully account for reproducing these statistical features in data of real bursting spike sequences. We resolve this difficulty by proposing an alternative neuron model which is a reduction of the bursting neuron model involving the persistent sodium current. Our study implies that (1) the characteristic features of CV and LV are the results of the endogenous bursting and (2) the bursting behavior in the gustatory cortex is caused mainly by the persistent sodium current.

Animals↗

PubMed2006

Dual coding hypotheses for neural information representation.

Information is represented and processed in neural systems in various ways. The rate coding, population coding, and temporal coding are typical examples of representation. It is a hot issue in neuroscience what kinds of coding is used in real neural systems. Different regions of the brain may resort to different coding strategies. Moreover, recent studies suggest the possibility of dual or multiple codes, in which different modes of information are embedded in one neural system. The present paper reviews various possibilities of neural codes focusing on dual codes.

Action Potentials↗

PubMed2006

Fisher information for spike-based population decoding.

We evaluate the Fisher information of a population of model neurons that receive dynamical input and interact via spikes. With spatially independent threshold noise, the spike-based Fisher information that summarizes the information carried by individual spike timings has a particularly simple analytical form. We calculate the loss of information caused by abandoning spike timing and study the effect of synaptic connections on the Fisher information. For a simple spatiotemporal input, we derive the optimal recurrent connectivity that has a local excitation and global inhibition structure. The optimal synaptic connections depend on the spatial or temporal feature of the input that the system is designed to code.

Algorithms↗

PubMed2006

Dynamic switching of neural codes in networks with gap junctions.

Population rate coding and temporal coding are common neural codes. Recent studies suggest that these two codes may be alternatively used in one neural system. Based on the fact that there are massive gap junctions in the brain, we explore how this switching behavior may be related to neural codes in networks of neurons connected by gap junctions. First, we show that under time-varying inputs, such neural networks show switching between synchronous and asynchronous states. Then, we quantify network dynamics by three mutual information measures to show that population rate coding carries more information in asynchronous states and temporal coding does so in synchronous states.

Action Potentials↗

PubMed2006

Reconstructing state spaces from multivariate data using variable delays.

We study two methods for constructing a nonuniform embedding for multivariate data. A nonuniform embedding is a state space reconstruction which is more flexible than the common delay coordinates with fixed delays since it contains variable delays. Using these methods, we can extract causal relationships among many variables in a more suitable way. We demonstrate that the proposed methods can give more precise predictions and simpler models than some previous methods.

Journal Article↗

PubMed2006

Transient resetting: a novel mechanism for synchrony and its biological examples.

The study of synchronization in biological systems is essential for the understanding of the rhythmic phenomena of living organisms at both molecular and cellular levels. In this paper, by using simple dynamical systems theory, we present a novel mechanism, named transient resetting, for the synchronization of uncoupled biological oscillators with stimuli. This mechanism not only can unify and extend many existing results on (deterministic and stochastic) stimulus-induced synchrony, but also may actually play an important role in biological rhythms. We argue that transient resetting is a possible mechanism for the synchronization in many biological organisms, which might also be further used in the medical therapy of rhythmic disorders. Examples of the synchronization of neural and circadian oscillators as well as a chaotic neuron model are presented to verify our hypothesis.

Action Potentials↗

PubMed2006

An optimal number of molecules for signal amplification and discrimination in a chemical cascade.

Understanding the information processing ability of signal transduction pathways is of great importance because of their crucial roles in triggering various cellular responses. Despite continuing theoretical investigation, some important aspects of signal transduction such as a transient response and its connection to stochasticity originating from a small number of molecules have not yet been well understood. It is, however, through these aspects that unexpected and nontrivial properties of the information processing emerge. In this article, we analyze the transient behavior of a simple signaling cascade by taking into account the stochasticity originating from the small number of molecules. We identify several properties of the signaling cascade that emerge as a result of the interplay between the stochasticity and transient dynamics of the cascade. We specifically demonstrate that each step of the cascade has an optimal number of signaling molecules at which the average signal amplitude becomes maximal. We further investigate the connection between a finite number of molecules and the ability of the cascade to discriminate between true and error signals, which cannot be inferred from deterministic descriptions. The implications of our results are discussed from both biological and mathematical viewpoints.

Computer Simulation↗

PubMed2006

A model for the circadian rhythm of cyanobacteria that maintains oscillation without gene expression.

An intriguing property of the cyanobacterial circadian clock is that endogenous rhythm persists when protein abundances are kept constant either in the presence of translation and transcription inhibitors or in the constant dark condition. Here we propose a regulatory mechanism of KaiC phosphorylation for the generation of circadian oscillations in cyanobacteria. In the model, clock proteins KaiA and KaiB are assumed to have multiple states, regulating the KaiC phosphorylation process. The model can explain 1), the sustained oscillation of gene expression and protein abundance when the expression of the kaiBC gene is regulated by KaiC protein, and 2), the sustained oscillation of phosphorylated KaiC when transcription and translation processes are inhibited and total protein abundance is fixed. Results of this work suggest that KaiA and KaiB strengthen the nonlinearity of KaiC phosphorylation, thereby promoting the circadian rhythm in cyanobacteria.

Bacterial Proteins↗

PubMed2006

Synchronizing a multicellular system by external input: an artificial control strategy.

MOTIVATION: Although there are significant advances on elucidating the collective behaviors on biological organisms in recent years, the essential mechanisms by which the collective rhythms arise remain to be fully understood, and further how to synchronize multicellular networks by artificial control strategy has not yet been well explored. RESULTS: A control strategy is developed to synchronize gene regulatory networks in a multicellular system when spontaneous synchronization cannot be achieved. We first construct an impulsive control system to model the process of periodically injecting coupling substances with constant or random impulsive control amounts into the common extracellular medium, and further study its effects on the dynamics of individual cells. We derive the threshold of synchronization induced by the periodic substance input. Therefore, we can synchronize the multicellular network to a specific collective behavior by changing the frequency and amplitude of the periodic stimuli. Moreover, a two-stage scheme is proposed to facilitate the synchronization in this paper. We show that the presence of the external input may also initiate different dynamics. The multicellular network of coupled repressilators is used to show the effectiveness of the proposed method. The results not only provide a perspective to understand the interactions between external stimuli and intrinsic physiological rhythms, but also may lead to development of realistic artificial control strategy and medical therapy. AVAILABILITY CONTACT: aihara@sat.t.u-tokyo.ac.jp.

Animals↗

PubMed2006

Synchronization of eukaryotic cells by periodic forcing.

We study a cell population described by a minimal mathematical model of the eukaryotic cell cycle subject to periodic forcing that simultaneously perturbs the dynamics of the cell cycle engine and cell growth, and we show that the population can be synchronized in a mode-locked regime. By simplifying the model to two variables, for the phase of cell cycle progression and the mass of the cell, we calculate the Lyapunov exponents to obtain the parameter window for synchronization. We also discuss the effects of intrinsic mitotic fluctuations, asymmetric division, and weak mutual coupling on the pace of synchronization.

Biomechanical Phenomena↗

PubMed2006

Construction of genetic oscillators with interlocked feedback networks.

To understand how a gene regulatory network functioning as an oscillator is built, a precise mathematical description of the network and its dynamical properties are developed in this paper. Our approach is based on analyzing the effect of interactions between smaller subnetworks with simple dynamics. We relate an oscillatory behavior of the network to the destabilization phenomenon of a steady state caused by the interactions in a simple discrete map. When source of the instability of the steady state rather than the oscillatory behavior itself is considered, linear stability analysis and feedback control theory can be employed. Moreover, the amplitudes robust against change in delay can also be obtained from the discrete map. The main ideas are illustrated by constructing a genetic oscillator termed a "repressilator" and analyzing the occurrence of cellular rhythms, although the theoretical results hold for a general class of biological systems. The method can be directly applied to design, construct genetic oscillators, and further control their dynamics, even for large-scale networks.

Animals↗

PubMed2006

Synchronization of coupled nonidentical genetic oscillators.

The study of the collective dynamics of synchronization among genetic oscillators is essential for the understanding of the rhythmic phenomena of living organisms at both molecular and cellular levels. Genetic oscillators are biochemical networks, which can generally be modelled as nonlinear dynamic systems. We show in this paper that many genetic oscillators can be transformed into Lur'e form by exploiting the special structure of biological systems. By using a control theory approach, we provide a theoretical method for analysing the synchronization of coupled nonidentical genetic oscillators. Sufficient conditions for the synchronization as well as the estimation of the bound of the synchronization error are also obtained. To demonstrate the effectiveness of our theoretical results, a population of genetic oscillators based on the Goodwin model are adopted as numerical examples.

Biological Clocks↗

PubMed2006

Synchronization and propagation of bursts in networks of coupled map neurons.

The present paper studies regular and complex spatiotemporal behaviors in networks of coupled map-based bursting oscillators. In-phase and antiphase synchronization of bursts are studied, explaining their underlying mechanisms in order to determine how network parameters separate them. Conditions for emergent bursting in the coupled system are derived from our analysis. In the region of emergence, patterns of chaotic transitions between synchronization and propagation of bursts are found. We show that they consist of transient standing and rotating waves induced by symmetry-breaking bifurcations, and can be viewed as a manifestation of the phenomenon of chaotic itinerancy.

Action Potentials↗

PubMed2006

Amelioration of ischemia/reperfusion-induced myocardial infarction by the 2-alkynyladenosine derivative 2-octynyladenosine (YT-146).

The present study was aimed at determining whether the novel adenosine A2-agonist YT-146 may have cardioprotective effects against ischemia-reperfusion injury. Anesthetized open-chest dogs underwent 90-min occlusion of the left anterior descending artery and subsequent 300-min reperfusion. The animals were randomly assigned to receive vehicle, 3, or 10 microg/kg YT-146 or ischemic preconditioning (4 episodes of 5 min occlusion followed by 5 min of reperfusion). Blood pressure, heart rate, and regional myocardial blood flow throughout the experiment were measured, as was the myocardial infarct size after reperfusion. The infarct size of the vehicle-treated dog was 56.2% +/- 2.7% (n = 5), whereas that of 3 or 10 microg/kg YT-146-treated dog was smaller (ie, 29.5% +/- 8.7% or 20.2% +/- 7.0%, respectively; n = 5). The infarct size of the dog treated with 10 microg/kg YT-146 was reduced to a degree similar to that of the ischemic preconditioning (19.2% +/- 6.3%, n = 5). YT-146 at both doses elicited a dose-dependent increase in acute hyperemic coronary flow immediately after reperfusion. The cardioprotective effect may be attributed to the limitation of the infarct size, probably via A2-receptor-mediated coronary artery dilatation during the early period of reperfusion.

Adenosine↗

PubMed2005

Bidirectional modulation of neuronal responses by depolarizing GABAergic inputs.

The reversal potential of GABAA receptor channels is known to be less negative than the resting membrane potential under some cases. Recent electrophysiological experiments revealed that a GABAergic unitary conductance with such a depolarized reversal potential could not only prevent but also facilitate action potential generation depending on the timing of its application relative to the excitatory unitary conductance. Using a two-dimensional point neuron model, we simulate the experiments regarding the integration of unitary conductances, and execute bifurcation analysis. Then we extend our analysis to the case in which the neuron receives two kinds of periodic input trains-an excitatory one and a GABAergic one. We show that the periodic depolarizing GABAergic input train can modulate the output time-averaged firing rate bidirectionally, namely as an increase or a decrease, in a devil's-staircase-like manner depending on the phase difference with the excitatory input train. Bifurcation analysis reveals the existence of a wide variety of phase-locked solutions underlying such a graded response of the neuron. We examine how the input time-width and the value of the GABAA reversal potential affect the response. Moreover, considering a neuronal population, we show that depolarizing GABAergic inputs bidirectionally modulate the amplitude of the oscillatory population activity.

Action Potentials↗

PubMed2005

Molecular communication through stochastic synchronization induced by extracellular fluctuations.

We model a synthetic gene regulatory network in a microbial cell, and investigate the effect of noises on cell-cell communication in a well-mixed multicellular system. A biologically plausible model is developed for cellular communication in an indirectly coupled multicellular system. Without extracellular noises, all cells, in spite of interaction among them, behave irregularly due to independent intracellular noises. On the other hand, extracellular noises that are common to all cells can induce collective dynamics and stochastically synchronize the multicellular system by actively enhancing the integrated interchange of signaling molecules.

Aliivibrio fischeri↗

PubMed2005

Bifurcations in a mathematical model for circadian oscillations of clock genes.

Circadian oscillations with a period of about 24h are observed in nearly all living organisms as conspicuous biological rhythms. In this paper, we investigate various kinds of bifurcation phenomena produced in a circadian oscillator model of Drosophila. In Drosophila, it is known that circadian oscillations in the levels of two proteins, PER and TIM, result from the negative feedback exerted by a PER-TIM complex on the expression of the per and tim genes that code for the two proteins. For studying circadian oscillations of proteins in Drosophila, a mathematical model has been proposed. The model cannot only account for regular circadian oscillations in environmental conditions such as constant darkness, but also give rise to more complex oscillatory phenomena including chaos and birhythmicity. By calculating bifurcations using Kawakami's method, we obtain detailed bifurcation diagrams related to stable and unstable invariant sets, and identify parameter regions in which the model generates complex oscillations as well as regular circadian oscillations. Moreover, we study bifurcations observed in the model incorporating the effect on a light-dark (LD) cycle and show that the waveform of the periodic variation in the light-induced parameter has a marked influence on the global bifurcation structure or the type of dynamic behavior resulting from the forcing term of the circadian oscillator by the LD cycles.

Animals↗

PubMed2005

Stochastic resonance of localized activity driven by common noise.

We study the influence of spatially correlated noise on the transient dynamics of a recurrent network with Mexican-Hat-type connectivity. We derive the closed form of the order parameter functional in the thermodynamical limit of neuron number N. Our analysis shows that network dynamics is qualitatively changed by the presence of common noise. Network dynamics driven by common noise obtains the global level of fluctuation, which is not observed in a network driven by independent noise only. We show that the optimal level of global fluctuation enhances the transition from non-localized firing states to spatially localized firing states, and also enhances the rotation speed of localized activity.

Brain↗