快自突触反馈诱发混合簇放电的反常变化及分岔机制

簇放电是神经系统复杂的、多时间尺度的非线性现象,具有多样性,在兴奋性或抑制性作用下实现生理功能.近期较多研究发现了与通常概念(抑制性作用引起电活动降低、兴奋性作用引起放电增强)相反的现象,丰富了非线性科学的内涵.本文关注于抑制性和兴奋性自突触反馈都会诱发的一类复杂的混合簇放电产生的反常现象及其分岔机制.利用快慢变量分离,确认了放电的复杂之处:簇结束于极限环的鞍结分岔之后要先经过去极化阻滞才到休止期.进一步,揭示了该鞍结分岔在反常现象的产生中起到了关键作用.抑制性自反馈引起了该分岔的左移导致簇的参数范围变宽,引起簇内峰个数增多和平均放电频率增加;而兴奋性自突触则引起该分岔右移导致电活动降低.与其他类簇放电只在抑制性自反馈下产生反常现象和慢突触诱发的反常现象不同,该结果给出了簇放电的反常现象的新示例及调控机制,展示了反常现象的多样性,有助于认识脑神经元簇放电和自反馈调控的潜在功能.     

计算相位响应曲线的方波扰动直接算法

通过相位响应曲线可对具有极限环周期运动的动力系统的性质有更为深入的理解.神经元是一个典型的动力系统,因此相位响应曲线提供了一种研究神经元重复周期放电行为的新思路.本文提出一种求解相位响应曲线的方法,即方波扰动的直接算法,通过Hodgkin-Huxley,Fitz Hugh-Nagumo,Morris-Lecar和Hindmarsh-Rose神经元模型验证该算法可计算周期峰放电、周期簇放电的相位响应曲线.该算法克服了其他算法在运用过程中的局限性.利用该算法计算结果表明:周期峰放电的相位响应曲线类型是由其分岔类型所决定;在Morris-Lecar模型中发现一种开始于Hopf分岔终止于鞍点同宿轨道分岔的阈上周期振荡,其相位响应曲线属于第二类型.通过大量的相位响应曲线的计算发现相位响应的相对大小及正负性仅取决于扰动所施加的时间,而且周期簇放电的相位响应曲线比周期峰放电的相位响应曲线更为复杂.     

兴奋性自突触引起神经簇放电频率降低或增加的非线性机制

兴奋和抑制性作用分别会增强和压制神经电活动,这是神经调控的通常观念,在神经信息处理中起重要作用.本文选取了放电簇和阈下振荡相交替、放电簇谷值小于阈下振荡谷值的Homoclinic/Homoclinic型簇放电,研究发现时滞和强度合适的兴奋性自突触电流作用在放电簇的谷值附近时,能引起簇内放电个数降低,并进而导致平均放电频率降低,这是不同于通常观念的新现象.进一步,用快慢变量分离获得的分岔和相轨迹,揭示了阈下振荡和放电簇分别对应快子系统的阈下和阈上极限环,兴奋性自突触电流引起阈上极限环向阈下极限环的转迁导致放电提前结束是频率降低原因.并与近期在Fold/Homoclinic簇放电报道的兴奋性自突触诱发的簇内放电个数降低但放电频率增加的现象和机制进行了比较.研究结果丰富了神经电活动的反常现象并揭示了背后的非线性机制,给出了调控簇放电的新手段,揭示了兴奋性自突触的潜在功能.     

Pre-B?tzinger复合体的从簇到峰放电的同步转迁及分岔机制

Pre-Bötzinger复合体是兴奋性耦合的神经元网络,通过产生复杂的放电节律和节律模式的同步转迁参与调控呼吸节律.本文选用复杂簇和峰放电节律的单神经元数学模型构建复合体模型,仿真了与生物学实验相关的多类同步节律模式及其复杂转迁历程,并利用快慢变量分离揭示了相应的分岔机制.当初值相同时,随着兴奋性耦合强度的增加,复合体模型依次表现出完全同步的“fold/homoclinic”,“subHopf/subHopf”簇放电和周期1峰放电.当初值不同时,随耦合强度增加,表现为由“fold/homoclinic”,到“fold/fold limit cycle”、到“subHopf/subHopf”与“fold/fold limit cycle”的混合簇放电、再到“subHopf/subHopf”簇放电的相位同步转迁,最后到反相同步周期1峰放电.完全(同相)同步和反相同步的周期1节律表现出了不同分岔机制.反相峰同步行为给出了与强兴奋性耦合容易诱发同相同步这一传统观念不同的新示例.研究结果给出了preBötzinger复合体的从簇到峰放电节律的同步转迁规律及复杂分岔机制,反常同步行为丰富了非线性动力学的内涵.     

相位噪声诱发神经放电的单次或两次相干共振

神经元电活动可以从静息通过Hopf分岔到放电,放电频率有固定周期;也可以从静息通过鞍-结分岔到放电,放电频率接近零.在具有周期性的相位噪声作用下的Hopf分岔和鞍-结分岔点附近,都会产生相干共振.噪声的周期小于Hopf分岔点附近的放电的周期时,相位噪声可以引起神经系统产生一次相干共振,位于系统内在的固有频率附近;噪声的周期大于系统的固有周期时,相位噪声可以引起双共振,对应低噪声强度的共振产生在噪声频率附近,对应高噪声强度的共振产生在系统的固有频率附近;并对双共振的产生原因进行了解释.在鞍-结分岔点附近,无论噪声的周期是大是小,都只会引起一次共振,研究结果不仅揭示了相位噪声作用下平衡点分岔点相干共振的动力学特性和对应于两类分岔的两类神经兴奋性的差别,还对近期的相位噪声诱发产生单或双共振的不同研究结果给出了解释.     

兴奋性和抑制性自反馈压制靠近Hopf分岔的神经电活动比较

突触输入刺激神经元产生的电活动,在神经编码中发挥着重要作用.通常认为,兴奋性输入增强电活动,抑制性输入压制电活动.本文选取可调节电流衰减速度的突触模型,研究了兴奋性自突触在亚临界Hopf分岔附近压制神经元电活动的反常作用,与抑制性自突触的压制作用进行了比较,并采用相位响应曲线和相平面分析解释了压制作用的机制.对于单稳的峰放电,快速和中速衰减的兴奋性自突触分别可以诱发频率降低的峰放电和混合振荡(峰放电与阈下振荡的交替),而中速和慢速衰减的抑制性自突触也可以分别诱发频率降低的峰放电和混合振荡.对于与静息共存的峰放电,除上述两种行为外,中速衰减的兴奋性和慢速衰减的抑制性自突触还可以诱发静息.兴奋性和抑制性自突触电流在不同的衰减速度下,分别作用在峰放电的不同相位,才能诱发同类压制行为.结果丰富了兴奋性突触压制电活动反常作用的实例,获得了兴奋性和抑制性自突触压制作用机制的不同,给出了调控神经放电的新手段.     

铂族金属氧化过程中的簇发振荡及其诱发机理

铂族金属表面氧化过程是典型的多相催化反应之一, 具有广泛的应用背景及丰富的振荡行为, 因此深入研究铂族金属的氧化中的物理及化学过程具有重要的理论意义及工程应用前景. 通过对铂族金属CO的氧化过程中实测数据的回归分析, 建立了不同尺度耦合解析动力学理论模型. 通过对平衡态的稳定性分析, 指出在一定条件下稳态解会由鞍-结同宿轨道分岔导致周期振荡. 当快子系统产生Hopf分岔时, 该周期振荡会进一步演化为两尺度耦合的周期簇发振荡, 即N^k振荡, 并由加周期分岔使得系统处于激发态的时间显著增加.在此基础上, 利用分岔理论进一步分析了周期簇发及加周期分岔的产生机理, 揭示了周期簇发中沉寂态和激发态相互转化时的不同分岔模式.     

具有时滞的抑制性自突触诱发的神经放电的加周期分岔

神经放电节律在神经系统功能实现中起着重要的作用.具有自突触(起始和结束于同一细胞的突触)的神经元普遍存在于神经系统,本文研究了单神经元模型在抑制性自突触作用下的放电节律.结果发现,随着时滞和/或耦合强度的增加,可以诱发Rulkov神经元模型放电节律的加周期分岔.随着放电节律的周期数的增加,平均放电频率增大,当时滞和/或耦合强度大于某一阈值时,频率大于没有自突触时的放电频率.用快慢变量分离方法可以获得没有自突触的神经放电节律的分岔结构,可用于认识外界负向脉冲诱发的新节律.这些新的节律模式与加周期分岔中的节律模式一致.研究结果不仅揭示了抑制性自突触可以诱发典型的非线性现象——加周期分岔,还给出了抑制性自突触可以提高放电频率的新现象,与以前的自突触压制放电的观点不同,进一步丰富了对抑制性自突触诱发的非线性现象的认识.     

双参数分岔平面内胰腺β细胞的簇放电分析

胰岛分泌胰岛素的放电活动以动作电位的簇放电为主要特点.文章考虑具有代表性且较为简单的Vries-Sherman模型,通过其快子系统的双参数分岔分析确定了双参数平面内不同簇放电类型的存在区域,并应用快慢动力学分析研究了参数v_m取不同值时所产生的簇放电模式的拓扑类型以及它们之间相互转迁的动力学机理. 关键词： 簇放电 快慢动力学 余维-2分岔     

连续时间系统同宿轨的搜索算法及其应用

同宿轨的求解是非线性系统领域的核心问题之一, 特别是对动力系统分岔与混沌的研究有重要意义. 根据同宿轨的几何特点, 采用轨线逼近的方式, 通过定义逼近轨线与鞍点的距离, 将同宿轨的求解转化为求距离最小值的无约束非线性优化问题. 为了提高优化结果的完整性, 还提出了基于区间细分的搜索算法和实现方法, 并找出了Lorenz系统, Shimizu-Morioka系统和超混沌Lorenz系统等的多个同宿轨道和对应参数, 验证了本文方法的有效性. 关键词： 混沌 同宿轨 非线性系统 数值计算     

Delayed excitatory self-feedback-induced negative responses of complex neuronal bursting patterns

In traditional viewpoint, excitatory modulation always promotes neural firing activities. On contrary, the negative responses of complex bursting behaviors to excitatory self-feedback mediated by autapse with time delay are acquired in the present paper. Two representative bursting patterns which are identified respectively to be "Fold/Big Homoclinic"bursting and "Circle/Fold cycle" bursting with bifurcations are studied. For both burstings, excitatory modulation can induce less spikes per burst for suitable time delay and strength of the self-feedback/autapse, because the modulation can change the initial or termination phases of the burst. For the former bursting composed of quiescent state and burst, the mean firing frequency exhibits increase, due to that the quiescent state becomes much shorter than the burst. However, for the latter bursting pattern with more complex behavior which is depolarization block lying between burst and quiescent state, the firing frequency manifests decrease in a wide range of time delay and strength, because the duration of both depolarization block and quiescent state becomes long. Therefore, the decrease degree of spike number per burst is larger than that of the bursting period, which is the cause for the decrease of firing frequency. Such reduced bursting activity is explained with the relations between the bifurcation points of the fast subsystem and the bursting trajectory. The present paper provides novel examples of paradoxical phenomenon that the excitatory effect induces negative responses, which presents possible novel modulation measures and potential functions of excitatory self-feedback/autapse to reduce bursting activities.     

Homoclinic bifurcations leading to the emergence of bursting oscillations in cell models

We present a qualitative analysis of a generic model structure that can simulate the bursting and spiking dynamics of many biological cells. Four different scenarios for the emergence of bursting are described. In this connection a number of theorems are stated concerning the relation between the phase portraits of the fast subsystem and the global behavior of the full model. It is emphasized that the onset of bursting involves the formation of a homoclinic orbit that travels along the route of the bursting oscillations and, hence, cannot be explained in terms of bifurcations in the fast subsystem. In one of the scenarios, the bursting oscillations arise in a homoclinic bifurcation in which the one-dimensional (1D) stable manifold of a saddle point becomes attracting to its whole 2D unstable manifold. This type of homoclinic bifurcation, and the complex behavior that it can produce, have not previously been examined in detail. We derive a 2D flow-defined map for this situation and show how the map transforms a disk-shaped cross-section of the flow into an annulus. Preliminary investigations of the stable dynamics of this map show that it produces an interesting cascade of alternating pitchfork and boundary collision bifurcations. Received 24 June 1999 and Received in final form 17 February 2000     

Transition between tonic spiking and bursting in a neuron model via the blue-sky catastrophe

We study a continuous and reversible transition between periodic tonic spiking and bursting activities in a neuron model. It is described as the blue-sky catastrophe, which is a homoclinic bifurcation of a saddle-node periodic orbit of codimension one. This transition constitutes a biophysically plausible mechanism for the regulation of burst duration that increases with no bound like 1/square root alpha-alpha0 as the transition value alpha0 is approached.     

Bursting and spiking due to additional direct and stochastic currents in neuron models

Neurons at rest can exhibit diverse firing activities patterns in response to various external deterministic and random stimuli, especially additional currents. In this paper, neuronal firing patterns from bursting to spiking, induced by additional direct and stochastic currents, are explored in rest states corresponding to two values of the parameter $V_{\rm K}$ in the Chay neuron system. Three cases are considered by numerical simulation and fast/slow dynamic analysis, in which only the direct current or the stochastic current exists, or the direct and stochastic currents coexist. Meanwhile, several important bursting patterns in neuronal experiments, such as the period-1 ``circle/homoclinic" bursting and the integer multiple ``fold/homoclinic" bursting with one spike per burst, as well as the transition from integer multiple bursting to period-1 ``circle/homoclinic" bursting and that from stochastic ``Hopf/homoclinic" bursting to ``Hopf/homoclinic" bursting, are investigated in detail.     

Origin of bursting through homoclinic spike adding in a neuron model

The origin of spike adding in bursting activity is studied in a reduced model of the leech heart interneuron. We show that, as the activation kinetics of the slow potassium current are shifted towards depolarized membrane potential values, the bursting phase accommodates incrementally more spikes into the train. This phenomenon is attested to be caused by the homoclinic bifurcations of a saddle periodic orbit setting the threshold between the tonic spiking and quiescent phases of the bursting. The fundamentals of the mechanism are revealed through the analysis of a family of the onto Poincaré return mappings.     

Bifurcations near homoclinic orbits with symmetry

The effect of symmetry on bifurcations associated with homoclinic orbits to saddle-foci is analysed. With symmetry each homoclinic bifurcation contributes three periodic orbits to the global bifurcation picture as opposed to a single orbit in the general case. Bifurcations on these orbits are studied: there are sequences of saddle-node and period-doubling bifurcations, chaos and more complicated homoclinic orbits.     

可兴奋性细胞混沌放电区间的识别机理

在神经起步点记录到加周期分岔过程的生理实验数据，在对此分岔过程中位于周期n爆发 和周期(n+1)爆发之间的混沌的峰峰间期数据检测不稳定的周期轨道时，发现从靠近周期 n爆发的混沌的峰峰间期数据中，可以检测出不稳定的周期n轨道；而从靠近周期(n+1)爆 发的混沌的峰峰间期数据中，不仅可以检测出不稳定的周期(n+1)轨道，还可以检测出不稳 定的周期n轨道.针对该现象，借助于Sherman建议的胰腺β细胞模型，从非线性动力 学角度给出了理论解释.指明了由鞍结分岔和倍周期分岔分别产生第一类阵发和第三类阵发 为出现该 关键词： 峰峰间期 不稳定的周期轨道 鞍结分岔 倍周期分岔