Spike-Timing Dependent Plasticity and Feed-Forward Input Oscillations Produce Precise and Invariant Spike Phase-Locking

In the hippocampus and the neocortex, the coupling between local field potential (LFP) oscillations and the spiking of single neurons can be highly precise, across neuronal populations and cell types. Spike phase (i.e., the spike time with respect to a reference oscillation) is known to carry reliable information, both with phase-locking behavior and with more complex phase relationships, such as phase precession. How this precision is achieved by neuronal populations, whose membrane properties and total input may be quite heterogeneous, is nevertheless unknown. In this note, we investigate a simple mechanism for learning precise LFP-to-spike coupling in feed-forward networks – the reliable, periodic modulation of presynaptic firing rates during oscillations, coupled with spike-timing dependent plasticity. When oscillations are within the biological range (2–150 Hz), firing rates of the inputs change on a timescale highly relevant to spike-timing dependent plasticity (STDP). Through analytic and computational methods, we find points of stable phase-locking for a neuron with plastic input synapses. These points correspond to precise phase-locking behavior in the feed-forward network. The location of these points depends on the oscillation frequency of the inputs, the STDP time constants, and the balance of potentiation and de-potentiation in the STDP rule. For a given input oscillation, the balance of potentiation and de-potentiation in the STDP rule is the critical parameter that determines the phase at which an output neuron will learn to spike. These findings are robust to changes in intrinsic post-synaptic properties. Finally, we discuss implications of this mechanism for stable learning of spike-timing in the hippocampus

On a link between Dirichlet kernels and central multinomial coefficients

AbstractThe central coefficients of powers of certain polynomials with arbitrary degree in x form an important family of integer sequences. Although various recursive equations addressing these coefficients do exist, no explicit analytic representation has yet been proposed. In this article, we present an explicit form of the integer sequences of central multinomial coefficients of polynomials of even degree in terms of finite sums over Dirichlet kernels, hence linking these sequences to discrete nth-degree Fourier series expansions. The approach utilizes the diagonalization of circulant Boolean matrices, and is generalizable to all multinomial coefficients of certain polynomials with even degree, thus forming the base for a new family of combinatorial identities

Theory of transient chimeras in finite Sakaguchi-Kuramoto networks

Chimera states are a phenomenon in which order and disorder can co-exist within a network that is fully homogeneous. Precisely how transient chimeras emerge in finite networks of Kuramoto oscillators with phase-lag remains unclear. Utilizing an operator-based framework to study nonlinear oscillator networks at finite scale, we reveal the spatiotemporal impact of the adjacency matrix eigenvectors on the Sakaguchi-Kuramoto dynamics. We identify a specific condition for the emergence of transient chimeras in these finite networks: the eigenvectors of the network adjacency matrix create a combination of a zero phase-offset mode and low spatial frequency waves traveling in opposite directions. This combination of eigenvectors leads directly to the coherent and incoherent clusters in the chimera. This approach provides two specific analytical predictions: (1) a precise formula predicting the combination of connectivity and phase-lag that creates transient chimeras, (2) a mathematical procedure for rewiring arbitrary networks to produce transient chimeras

Composed solutions of synchronized patterns in multiplex networks of Kuramoto oscillators

Networks with different levels of interactions, including multilayer and multiplex networks, can display a rich diversity of dynamical behaviors and can be used to model and study a wide range of systems. Despite numerous efforts to investigate these networks, obtaining mathematical descriptions for the dynamics of multilayer and multiplex systems is still an open problem. Here, we combine ideas and concepts from linear algebra and graph theory with nonlinear dynamics to offer a novel approach to study multiplex networks of Kuramoto oscillators. Our approach allows us to study the dynamics of a large, multiplex network by decomposing it into two smaller systems: one representing the connection scheme within layers (intra-layer), and the other representing the connections between layers (inter-layer). Particularly, we use this approach to compose solutions for multiplex networks of Kuramoto oscillators. These solutions are given by a combination of solutions for the smaller systems given by the intra and inter-layer system and, in addition, our approach allows us to study the linear stability of these solutions

Small changes at single nodes can shift global network dynamics

Understanding the sensitivity of a system's behavior with respect to parameter changes is essential for many applications. This sensitivity may be desired - for instance in the brain, where a large repertoire of different dynamics, particularly different synchronization patterns, is crucial - or may be undesired - for instance in power grids, where disruptions to synchronization may lead to blackouts. In this work, we show that the dynamics of networks of phase oscillators can acquire a very large and complex sensitivity to changes made in either their units' parameters or in their connections - even modifications made to a parameter of a single unit can radically alter the global dynamics of the network in an unpredictable manner. As a consequence, each modification leads to a different path to phase synchronization manifested as large fluctuations along that path. This dynamical malleability occurs over a wide parameter region, around the network's two transitions to phase synchronization. One transition is induced by increasing the coupling strength between the units, and another is induced by increasing the prevalence of long-range connections. Specifically, we study Kuramoto phase oscillators connected under either Watts-Strogatz or distance-dependent topologies to analyze the statistical properties of the fluctuations along the paths to phase synchrony. We argue that this increase in the dynamical malleability is a general phenomenon, as suggested by both previous studies and the theory of phase transitions.Comment: 14 pages, 8 figure

State-dependent activity dynamics of hypothalamic stress effector neurons

The stress response necessitates an immediate boost in vital physiological functions from their homeostatic operation to an elevated emergency response. However, the neural mechanisms underlying this state-dependent change remain largely unknown. Using a combination of in vivo and ex vivo electrophysiology with computational modeling, we report that corticotropin releasing hormone (CRH) neurons in the paraventricular nucleus of the hypothalamus (PVN), the effector neurons of hormonal stress response, rapidly transition between distinct activity states through recurrent inhibition. Specifically, in vivo optrode recording shows that under non-stress conditions, CRHPVN neurons often fire with rhythmic brief bursts (RB), which, somewhat counterintuitively, constrains firing rate due to long (~2 s) interburst intervals. Stressful stimuli rapidly switch RB to continuous single spiking (SS), permitting a large increase in firing rate. A spiking network model shows that recurrent inhibition can control this activity-state switch, and more broadly the gain of spiking responses to excitatory inputs. In biological CRHPVN neurons ex vivo, the injection of whole-cell currents derived from our computational model recreates the in vivo-like switch between RB and SS, providing direct evidence that physiologically relevant network inputs enable state-dependent computation in single neurons. Together, we present a novel mechanism for state-dependent activity dynamics in CRHPVN neurons