Potential mechanisms for imperfect synchronization in parkinsonian basal ganglia

Neural activity in the brain of parkinsonian patients is characterized by the intermittently synchronized oscillatory dynamics. This imperfect synchronization, observed in the beta frequency band, is believed to be related to the hypokinetic motor symptoms of the disorder. Our study explores potential mechanisms behind this intermittent synchrony. We study the response of a bursting pallidal neuron to different patterns of synaptic input from subthalamic nucleus (STN) neuron. We show how external globus pallidus (GPe) neuron is sensitive to the phase of the input from the STN cell and can exhibit intermittent phase-locking with the input in the beta band. The temporal properties of this intermittent phase-locking show similarities to the intermittent synchronization observed in experiments. We also study the synchronization of GPe cells to synaptic input from the STN cell with dependence on the dopamine-modulated parameters. Dopamine also affects the cellular properties of neurons. We show how the changes in firing patterns of STN neuron due to the lack of dopamine may lead to transition from a lower to a higher coherent state, roughly matching the synchrony levels observed in basal ganglia in normal and parkinsonian states. The intermittent nature of the neural beta band synchrony in Parkinson's disease is achieved in the model due to the interplay of the timing of STN input to pallidum and pallidal neuronal dynamics, resulting in sensitivity of pallidal output to the phase of the arriving STN input. Thus the mechanism considered here (the change in firing pattern of subthalamic neurons through the dopamine-induced change of membrane properties) may be one of the potential mechanisms responsible for the generation of the intermittent synchronization observed in Parkinson's disease.Comment: 27 pages, 9 figure

A Fast-Slow Analysis of the Dynamics of REM Sleep

Waking and sleep states are regulated by the coordinated activity of a number of neuronal population in the brainstem and hypothalamus whose synaptic interactions compose a sleep-wake regulatory network. Physiologically based mathematical models of the sleep-wake regulatory network contain mechanisms operating on multiple time scales including relatively fast synaptic-based interations between neuronal populations, and much slower homeostatic and circadian processes that modulate sleep-wake temporal patterning. In this study, we exploit the naturally arising slow time scale of the homeostatic sleep drive in a reduced sleep-wake regulatory network model to utilize fast-slow analysis to investigate the dynamics of rapid eye movement (REM) sleep regulation. The network model consists of a reduced number of wake-, non-REM (NREM) sleep-, and REM sleep-promoting neuronal populations with the synaptic interactions reflecting the mutually inhibitory flip-flop conceptual model for sleep-wake regulation and the reciprocal interaction model for REM sleep regulation. Network dynamics regularly alternate between wake and sleep states as goverend by the slow homeostatic sleep drive. By varying a parameter associated with the activation of the REM-promoting population, we cause REM dynamics during sleep episodes to vary from supression to single activations to regular REM-NREM cycling, corresponding to changes in REM patterning induced by circadian modulation and observed in different mammalian species. We also utilize fast-slow analysis to explain complex effects on sleep-wake patterning of simulated experiments in which agonists and antagonists of different neurotransmitters are microinjected into specific neuronal populations participating in the sleep-wake regulatory network

A note on Keen's model: The limits of Schumpeter's "Creative Destruction"

This paper presents a general solution for a recent model by Keen for endogenous money creation. The solution provides an analytic framework that explains all significant dynamical features of Keen's model and their parametric dependence, including an exact result for both the period and subsidence rate of the Great Moderation. It emerges that Keen's model has just two possible long term solutions: stable growth or terminal collapse. While collapse can come about immediately from economies that are nonviable by virtue of unsuitable parameters or initial conditions, in general the collapse is preceded by an interval of exponential growth. In first approximation, the duration of that exponential growth is half a period of a sinusoidal oscillation. The period is determined by reciprocal of the imaginary part of one root of a certain quintic polynomial. The real part of the same root determines the rate of growth of the economy. The coefficients of that polynomial depend in a complicated way upon the numerous parameters in the problem and so, therefore, the pattern of roots. For a favorable choice of parameters, the salient root is purely real. This is the circumstance that admits the second possible long term solution, that of indefinite stable growth, i.e. an infinite period.Comment: 25 pages, 12 figures, JEL classification: B50, C62, C63, E12, E4

High-feedback Operation of Power Electronic Converters

electronic

Complex and unexpected dynamics in simple genetic regulatory networks

Peer reviewedPublisher PD