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<abstract><p>Intrinsic bursting neurons represent a common neuronal type that displays bursting patterns upon depolarization stimulation. These neurons can be described by a system of seven-dimensional equations, which pose a challenge for dynamical analysis. To overcome this limitation, we employed the projection reduction method to reduce the dimensionality of the model. Our approach demonstrated that the reduced model retained the inherent bursting characteristics of the original model. Following reduction, we investigated the bi-parameter bifurcation of the equilibrium point in the reduced model. Specifically, we analyzed the Bogdanov-Takens bifurcation that arises in the reduced system. Notably, the topological structure of the neuronal model near the bifurcation point can be effectively revealed with our proposed method. By leveraging the proposed projection reduction method, we could explore the bursting mechanism in the reduced Pospischil model with greater precision. Our approach offers an effective foundation for generating theories and hypotheses that can be tested experimentally. Furthermore, it enables links to be drawn between neuronal morphology and function, thereby facilitating a deeper understanding of the complex dynamical behaviors that underlie intrinsic bursting neurons.</p></abstract>
<abstract><p>Intrinsic bursting neurons represent a common neuronal type that displays bursting patterns upon depolarization stimulation. These neurons can be described by a system of seven-dimensional equations, which pose a challenge for dynamical analysis. To overcome this limitation, we employed the projection reduction method to reduce the dimensionality of the model. Our approach demonstrated that the reduced model retained the inherent bursting characteristics of the original model. Following reduction, we investigated the bi-parameter bifurcation of the equilibrium point in the reduced model. Specifically, we analyzed the Bogdanov-Takens bifurcation that arises in the reduced system. Notably, the topological structure of the neuronal model near the bifurcation point can be effectively revealed with our proposed method. By leveraging the proposed projection reduction method, we could explore the bursting mechanism in the reduced Pospischil model with greater precision. Our approach offers an effective foundation for generating theories and hypotheses that can be tested experimentally. Furthermore, it enables links to be drawn between neuronal morphology and function, thereby facilitating a deeper understanding of the complex dynamical behaviors that underlie intrinsic bursting neurons.</p></abstract>
<abstract><p>Parkinson's disease is associated with bursting of the thalamic (TC) neuron, which receives the inhibitory synaptic current of the basal ganglia composed of multiple nuclei; deep brain stimulation (DBS) applied to the basal ganglia can eliminate the bursting to recover to the normal state. In this paper, the complex nonlinear dynamics for the appearance and disappearance of the bursting are obtained in a widely used theoretical model of a neuronal network. First, through a bifurcation analysis, isolated TC neurons exhibit paradoxical bursting induced from the resting state by enhanced inhibitory effect, which is different from the common view that the enhanced inhibitory effect should suppress the electrical behaviors. Second, the mechanism for the appearance of bursting is obtained by analyzing the electrical activities of the basal ganglia. The inhibitory synaptic current from the external segment of the globus pallidus (GPe) induces a reduced firing rate of the subthalamic nucleus (STN); then, an excitatory synaptic current from the STN induces the bursting behaviors of the GPe. The excitatory current of STN neurons and the inhibitory current of the GPe cause bursting behaviors of the internal segment of the globus pallidus (GPi), thus resulting in an enhanced inhibition from the GPi to the TC, which can induce the paradoxical bursting similar to the isolated TC neurons. Third, the cause for the disappearance of paradoxical bursting is acquired.The high frequency pulses of DBS induces enhanced firing activity of the STN and GPe neurons and enhanced inhibitory synaptic current from the GPe to the GPi, resulting in a reduced inhibitory effect from the GPi to the TC, which can eliminate the paradoxical bursting. Finally, the fast-slow dynamics of the paradoxical bursting of isolated TC neurons are acquired, which is related to the saddle-node and saddle-homoclinic orbit bifurcations of the fast subsystem of the TC neuron model. The results provide theoretical support for understanding the mechanism of Parkinson's disease and treatment methods such as DBS.</p></abstract>
The neocortex of the brain plays the most important role in achieving functions of the brain via the electrical activities of neurons. Understanding the transition regularity of firing patterns and underlying dynamics of firing patterns of neurons can help to identify the brain functions and to treat some brain diseases. Different neocortical neurons exhibit regular spiking (RS), fast spiking (FS), intrinsic bursting (IB), and continuous bursting (CB), which play vital roles and wide range of functions. Fast-slow variable dissection method combined with bifurcation analysis has been an effective method to identify underlying dynamical mechanism of spiking and bursting modulated by a single slow variable. The spiking is related to the stable limit cycle of the fast subsystem, and the bursting is associated with the transitions or bifurcations between the stable limit cycle and resting state of the fast subsystem. Such underlying dynamics of bursting have been widely used to distinguish different bursting patterns and identify complex dynamics of bursting modulated by various different factors such as synaptic current, autaptic current, and stimulations applied at a suitable phase related to the bifurcations, which play important roles in the real nervous system to regulate neural firing behaviors. Unfortunately, the bursting of neocortical neuronal model (Wilson model) is modulated by two slow variables, the gating variable of calcium-activated potassium channel <i>H</i> and the gating variable of T-type calcium channel <i>T</i>. <i>H</i> is slower than <i>T</i>. Then, the underlying dynamical mechanism of the IB and CB of the neocortical neurons cannot be acquired with fast-slow variable dissection method when <i>H</i> is taken as the sole slow variable, due to that the fast-subsystem contains the slow variable <i>T</i>. In the present paper, we use the fast-slow variable dissection method with two slow variables (<i>H</i> and <i>T</i>) to analyze the bursting patterns. The bifurcations of the fast subsystem, and the intersections between the bifurcation curves and the phase trajectory of bursting in the parameter plane (<i>H</i>, <i>T</i>) are acquired. Due to that neither of the two slow variables of the bursting is sufficiently slow, the bifurcations of only some intersections are related to the bursting behaviors whereas others not. Then, the position relationship between the bifurcation curves and bursting trajectory in the three-dimensional space (<i>H</i>, <i>T</i>, <i>V</i>) (<i>V</i> is membrane potential of bursting) is further acquired, from which the bifurcations related to bursting behaviors are acquired and bifurcations not associated with the bursting behaviors are excluded. The start and termination phases of the burst of the IB are related to the saddle-node on invariant circle (SNIC) bifurcation, and not to the saddle-node (SN) bifurcation. The start and termination phases of the burst of the CB are related to the SNIC bifurcation and the supercritical Andronov-Hopf (SupHopf) bifurcation, respectively, and not to the SN bifurcation. The results present a comprehensive and deep understanding of the underlying dynamics of bursting patterns in the neocortical neurons, which lay the foundation for regulating the firing patterns of the neocortical neurons.
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