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Register a new userNonlinear gap junctions enable long-distance propagation of pulsating calcium waves in astrocyte networks
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A new paradigm has recently emerged in brain science whereby communications between glial cells and neuron-glia interactions should be considered together with neurons and their networks to understand higher brain functions. In particular, astrocytes, the main type of glial cells in the cortex, have been shown to communicate with neurons and with each other. They are thought to form a gap-junction-coupled syncytium supporting cell-cell communication via propagating Ca2+ waves. An identified mode of propagation is based on cytoplasm-to-cytoplasm transport of inositol trisphosphate (IP3) through gap junctions that locally trigger Ca2+ pulses via IP3-dependent Ca2+-induced Ca2+ release. It is, however, currently unknown whether this intracellular route is able to support the propagation of long-distance regenerative Ca2+ waves or is restricted to short-distance signaling. Furthermore, the influence of the intracellular signaling dynamics on intercellular propagation remains to be understood. In this work, we propose a model of the gap-junctional route for intercellular Ca2+ wave propagation in astrocytes showing that: (1) long-distance regenerative signaling requires nonlinear coupling in the gap junctions, and (2) even with nonlinear gap junctions, long-distance regenerative signaling is favored when the internal Ca2+ dynamics implements frequency modulation-encoding oscillations with pulsating dynamics, while amplitude modulation-encoding dynamics tends to restrict the propagation range. As a result, spatially heterogeneous molecular properties and/or weak couplings are shown to give rise to rich spatiotemporal dynamics that support complex propagation behaviors. These results shed new light on the mechanisms implicated in the propagation of Ca2+ waves across astrocytes and precise the conditions under which glial cells may participate in information processing in the brain.
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Observability and controllability are essential concepts to the design of predictive observer models and feedback controllers of networked systems. For example, noncontrollable mathematical models of real systems have subspaces that influence model behavior, but cannot be controlled by an input. Such subspaces can be difficult to determine in complex nonlinear networks. Since almost all of the present theory was developed for linear networks without symmetries, here we present a numerical and group representational framework, to quantify the observability and controllability of nonlinear networks with explicit symmetries that shows the connection between symmetries and nonlinear measures of observability and controllability. We numerically observe and theoretically predict that not all symmetries have the same effect on network observation and control. Our analysis shows that the presence of symmetry in a network may decrease observability and controllability, although networks containing only rotational symmetries remain controllable and observable. These results alter our view of the nature of observability and controllability in complex networks, change our understanding of structural controllability, and affect the design of mathematical models to observe and control such networks.
Recent years have witnessed an increasing interest in neuron-glia communication. This interest stems from the realization that glia participates in cognitive functions and information processing and is involved in many brain disorders and neurodegenerative diseases. An important process in neuron-glia communications is astrocyte encoding of synaptic information transfer: the modulation of intracellular calcium dynamics in astrocytes in response to synaptic activity. Here, we derive and investigate a concise mathematical model for glutamate-induced astrocytic intracellular Ca2+ dynamics that captures the essential biochemical features of the regulatory pathway of inositol 1,4,5-trisphosphate (IP3). Starting from the well-known two-state Li-Rinzel model for calcium-induced-calcium release, we incorporate the regulation of the IP3 production and phosphorylation. Doing so we extended it to a three-state model (referred as the G-ChI model), that could account for Ca2+ oscillations triggered by endogenous IP3 metabolism as well as by IP3 production by external glutamate signals. Compared to previous similar models, our three-state models include a more realistic description of the IP3 production and degradation pathways, lumping together their essential nonlinearities within a concise formulation. Using bifurcation analysis and time simulations, we demonstrate the existence of new putative dynamical features. The cross-couplings between IP3 and Ca2+ pathways endows the system with self-consistent oscillator properties and favor mixed frequency-amplitude encoding modes over pure amplitude modulation ones. These and additional results of our model are in general agreement with available experimental data and may have important implications on the role of astrocytes in the synaptic transfer of information.
Macroscopic EEG fields can be an explicit top-down neocortical mechanism that directly drives bottom-up processes that describe memory, attention, and other neuronal processes. The top-down mechanism considered are macrocolumnar EEG firings in neocortex, as described by a statistical mechanics of neocortical interactions (SMNI), developed as a magnetic vector potential $mathbf{A}$. The bottom-up process considered are $mathrm{Ca}^{2+}$ waves prominent in synaptic and extracellular processes that are considered to greatly influence neuronal firings. Here, the complimentary effects are considered, i.e., the influence of $mathbf{A}$ on $mathrm{Ca}^{2+}$ momentum, $mathbf{p}$. The canonical momentum of a charged particle in an electromagnetic field, $mathbf{Pi} = mathbf{p} + q mathbf{A}$ (SI units), is calculated, where the charge of $mathrm{Ca}^{2+}$ is $q = - 2 e$, $e$ is the magnitude of the charge of an electron. Calculations demonstrate that macroscopic EEG $mathbf{A}$ can be quite influential on the momentum $mathbf{p}$ of $mathrm{Ca}^{2+}$ ions, in both classical and quantum mechanics. Molecular scales of $mathrm{Ca}^{2+}$ wave dynamics are coupled with $mathbf{A}$ fields developed at macroscopic regional scales measured by coherent neuronal firing activity measured by scalp EEG. The project has three main aspects: fitting $mathbf{A}$ models to EEG data as reported here, building tripartite models to develop $mathbf{A}$ models, and studying long coherence times of $mathrm{Ca}^{2+}$ waves in the presence of $mathbf{A}$ due to coherent neuronal firings measured by scalp EEG. The SMNI model supports a mechanism wherein the $mathbf{p} + q mathbf{A}$ interaction at tripartite synapses, via a dynamic centering mechanism (DCM) to control background synaptic activity, acts to maintain short-term memory (STM) during states of selective attention.
The Integrated Information is a quantitative measure from information theory how tightly all parts of a system are interconnected in terms of information exchange. In this study we show that astrocyte, playing an important role in regulation of information transmission between neurons, may contribute to a generation of positive Integrated Information in neuronal ensembles. Analytically and numerically we show that the presence of astrocyte may be essential for this information attribute in neuro-astrocytic ensembles. Moreover, the proposed spiking-bursting mechanism of generating positive Integrated Information is shown to be generic and not limited to neuroglial networks, and is given a complete analytic description.
Short-term presynaptic plasticity designates variations of the amplitude of synaptic information transfer whereby the amount of neurotransmitter released upon presynaptic stimulation changes over seconds as a function of the neuronal firing activity. While a consensus has emerged that changes of the synapse strength are crucial to neuronal computations, their modes of expression in vivo remain unclear. Recent experimental studies have reported that glial cells, particularly astrocytes in the hippocampus, are able to modulate short-term plasticity but the underlying mechanism is poorly understood. Here, we investigate the characteristics of short-term plasticity modulation by astrocytes using a biophysically realistic computational model. Mean-field analysis of the model unravels that astrocytes may mediate counterintuitive effects. Depending on the expressed presynaptic signaling pathways, astrocytes may globally inhibit or potentiate the synapse: the amount of released neurotransmitter in the presence of the astrocyte is transiently smaller or larger than in its absence. But this global effect usually coexists with the opposite local effect on paired pulses: with release-decreasing astrocytes most paired pulses become facilitated, while paired-pulse depression becomes prominent under release-increasing astrocytes. Moreover, we show that the frequency of astrocytic intracellular Ca2+ oscillations controls the effects of the astrocyte on short-term synaptic plasticity. Our model explains several experimental observations yet unsolved, and uncovers astrocytic gliotransmission as a possible transient switch between short-term paired-pulse depression and facilitation. This possibility has deep implications on the processing of neuronal spikes and resulting information transfer at synapses.
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