3,588 research outputs found
A biophysical model explains the spontaneous bursting behavior in the developing retina
During early development, waves of activity propagate across the retina and
play a key role in the proper wiring of the early visual system. During the
stage II these waves are triggered by a transient network of neurons, called
Starburst Amacrine Cells (SACs), showing a bursting activity which disappears
upon further maturation. While several models have attempted to reproduce
retinal waves, none of them is able to mimic the rhythmic autonomous bursting
of individual SACs and reveal how these cells change their intrinsic properties
during development. Here, we introduce a mathematical model, grounded on
biophysics, which enables us to reproduce the bursting activity of SACs and to
propose a plausible, generic and robust, mechanism that generates it. The core
parameters controlling repetitive firing are fast depolarizing -gated
calcium channels and hyperpolarizing -gated potassium channels. The
quiescent phase of bursting is controlled by a slow after hyperpolarization
(sAHP), mediated by calcium-dependent potassium channels. Based on a
bifurcation analysis we show how biophysical parameters, regulating calcium and
potassium activity, control the spontaneously occurring fast oscillatory
activity followed by long refractory periods in individual SACs. We make a
testable experimental prediction on the role of voltage-dependent potassium
channels on the excitability properties of SACs and on the evolution of this
excitability along development. We also propose an explanation on how SACs can
exhibit a large variability in their bursting periods, as observed
experimentally within a SACs network as well as across different species, yet
based on a simple, unique, mechanism. As we discuss, these observations at the
cellular level have a deep impact on the retinal waves description.Comment: 25 pages, 13 figures, submitte
Synchronous Behavior of Two Coupled Electronic Neurons
We report on experimental studies of synchronization phenomena in a pair of
analog electronic neurons (ENs). The ENs were designed to reproduce the
observed membrane voltage oscillations of isolated biological neurons from the
stomatogastric ganglion of the California spiny lobster Panulirus interruptus.
The ENs are simple analog circuits which integrate four dimensional
differential equations representing fast and slow subcellular mechanisms that
produce the characteristic regular/chaotic spiking-bursting behavior of these
cells. In this paper we study their dynamical behavior as we couple them in the
same configurations as we have done for their counterpart biological neurons.
The interconnections we use for these neural oscillators are both direct
electrical connections and excitatory and inhibitory chemical connections: each
realized by analog circuitry and suggested by biological examples. We provide
here quantitative evidence that the ENs and the biological neurons behave
similarly when coupled in the same manner. They each display well defined
bifurcations in their mutual synchronization and regularization. We report
briefly on an experiment on coupled biological neurons and four dimensional ENs
which provides further ground for testing the validity of our numerical and
electronic models of individual neural behavior. Our experiments as a whole
present interesting new examples of regularization and synchronization in
coupled nonlinear oscillators.Comment: 26 pages, 10 figure
The role of inhibitory feedback for information processing in thalamocortical circuits
The information transfer in the thalamus is blocked dynamically during sleep,
in conjunction with the occurence of spindle waves. As the theoretical
understanding of the mechanism remains incomplete, we analyze two modeling
approaches for a recent experiment by Le Masson {\sl et al}. on the
thalamocortical loop. In a first step, we use a conductance-based neuron model
to reproduce the experiment computationally. In a second step, we model the
same system by using an extended Hindmarsh-Rose model, and compare the results
with the conductance-based model. In the framework of both models, we
investigate the influence of inhibitory feedback on the information transfer in
a typical thalamocortical oscillator. We find that our extended Hindmarsh-Rose
neuron model, which is computationally less costly and thus siutable for
large-scale simulations, reproduces the experiment better than the
conductance-based model. Further, in agreement with the experiment of Le Masson
{\sl et al}., inhibitory feedback leads to stable self-sustained oscillations
which mask the incoming input, and thereby reduce the information transfer
significantly.Comment: 16 pages, 15eps figures included. To appear in Physical Review
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
Neuronal synchrony: peculiarity and generality
Synchronization in neuronal systems is a new and intriguing application of dynamical systems theory. Why are neuronal systems different as a subject for synchronization? (1) Neurons in themselves are multidimensional nonlinear systems that are able to exhibit a wide variety of different activity patterns. Their âdynamical repertoireâ includes regular or chaotic spiking, regular or chaotic bursting, multistability, and complex transient regimes. (2) Usually, neuronal oscillations are the result of the cooperative activity of many synaptically connected neurons (a neuronal circuit). Thus, it is necessary to consider synchronization between different neuronal circuits as well. (3) The synapses that implement the coupling between neurons are also dynamical elements and their intrinsic dynamics influences the process of synchronization or entrainment significantly. In this review we will focus on four new problems: (i) the synchronization in minimal neuronal networks with plastic synapses (synchronization with activity dependent coupling), (ii) synchronization of bursts that are generated by a group of nonsymmetrically coupled inhibitory neurons (heteroclinic synchronization), (iii) the coordination of activities of two coupled neuronal networks (partial synchronization of small composite structures), and (iv) coarse grained synchronization in larger systems (synchronization on a mesoscopic scale
Death and rebirth of neural activity in sparse inhibitory networks
In this paper, we clarify the mechanisms underlying a general phenomenon
present in pulse-coupled heterogeneous inhibitory networks: inhibition can
induce not only suppression of the neural activity, as expected, but it can
also promote neural reactivation. In particular, for globally coupled systems,
the number of firing neurons monotonically reduces upon increasing the strength
of inhibition (neurons' death). However, the random pruning of the connections
is able to reverse the action of inhibition, i.e. in a sparse network a
sufficiently strong synaptic strength can surprisingly promote, rather than
depress, the activity of the neurons (neurons' rebirth). Thus the number of
firing neurons reveals a minimum at some intermediate synaptic strength. We
show that this minimum signals a transition from a regime dominated by the
neurons with higher firing activity to a phase where all neurons are
effectively sub-threshold and their irregular firing is driven by current
fluctuations. We explain the origin of the transition by deriving an analytic
mean field formulation of the problem able to provide the fraction of active
neurons as well as the first two moments of their firing statistics. The
introduction of a synaptic time scale does not modify the main aspects of the
reported phenomenon. However, for sufficiently slow synapses the transition
becomes dramatic, the system passes from a perfectly regular evolution to an
irregular bursting dynamics. In this latter regime the model provides
predictions consistent with experimental findings for a specific class of
neurons, namely the medium spiny neurons in the striatum.Comment: 19 pages, 10 figures, submitted to NJ
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