Connectivity reflects coding: A model of voltage-based spike-timing-dependent-plasticity with homeostasis

Electrophysiological connectivity patterns in cortex often show a few strong connections in a sea of weak connections. In some brain areas a large fraction of strong connections are bidirectional, in others they are mainly unidirectional. In order to explain these connectivity patterns, we use a model of Spike-Timing-Dependent Plasticity where synaptic changes depend on presynaptic spike arrival and the postsynaptic membrane potential. The model describes several nonlinear effects in STDP experiments, as well as the voltage dependence of plasticity under voltage clamp and classical paradigms of LTP/LTD induction. We show that in a simulated recurrent network of spiking neurons our plasticity rule leads not only to receptive field development, but also to connectivity patterns that reflect the neural code: for temporal coding paradigms strong connections are predominantly unidirectional, whereas they are bidirectional under rate coding. Thus variable connectivity patterns in the brain could reflect different coding principles across brain areas

Extracting non-linear integrate-and-fire models from experimental data using dynamic I–V curves

The dynamic I–V curve method was recently introduced for the efficient experimental generation of reduced neuron models. The method extracts the response properties of a neuron while it is subject to a naturalistic stimulus that mimics in vivo-like fluctuating synaptic drive. The resulting history-dependent, transmembrane current is then projected onto a one-dimensional current–voltage relation that provides the basis for a tractable non-linear integrate-and-fire model. An attractive feature of the method is that it can be used in spike-triggered mode to quantify the distinct patterns of post-spike refractoriness seen in different classes of cortical neuron. The method is first illustrated using a conductance-based model and is then applied experimentally to generate reduced models of cortical layer-5 pyramidal cells and interneurons, in injected-current and injected- conductance protocols. The resulting low-dimensional neuron models—of the refractory exponential integrate-and-fire type—provide highly accurate predictions for spike-times. The method therefore provides a useful tool for the construction of tractable models and rapid experimental classification of cortical neurons

Pattern formation in oscillatory complex networks consisting of excitable nodes

Oscillatory dynamics of complex networks has recently attracted great attention. In this paper we study pattern formation in oscillatory complex networks consisting of excitable nodes. We find that there exist a few center nodes and small skeletons for most oscillations. Complicated and seemingly random oscillatory patterns can be viewed as well-organized target waves propagating from center nodes along the shortest paths, and the shortest loops passing through both the center nodes and their driver nodes play the role of oscillation sources. Analyzing simple skeletons we are able to understand and predict various essential properties of the oscillations and effectively modulate the oscillations. These methods and results will give insights into pattern formation in complex networks, and provide suggestive ideas for studying and controlling oscillations in neural networks.Comment: 15 pages, 7 figures, to appear in Phys. Rev.

Síndrome del túnel carpiano. Evaluación clínica y ayudas diagnósticas

  The Carpal tunnel syndrome is a compression of the median nerve at the level of the wrist. Symptoms include pain and paresthesia, especially at night, and improves with arm elevation and movement of the hand. Treatment begins with rest of the hand, anti inflammatory drugs and nocturnal splint in extension of the wrist. If there is not improvement, a corticoid injection with local anesthesia into the wrist can be used with improvement of symptoms.  Surgery is indicated in failed orthopaedic treatment, when nerve conduction studies show pathologic changes or if a sensitive o motor deficit is demonstrated. Surgery relieves pain but does not improve previous sensitive and motor deficits.  Keywords: Carpal tunnel syndrome. Median nerve. Compression neuropaty. El síndrome del túnel carpiano deriva de la compresión del nervio mediano a nivel de la muñeca. Los síntomas más frecuentes son dolor y parestesias de predominio nocturno con compromiso del sueño, que pueden ceder con elevación del brazo y agitación de la mano. El objetivo de este artículo es hacer una revisión actualizada del tema aunando la experiencia del autor. Puede iniciarse el tratamiento recomendando reposo de la mano, antinflamatorios no esteroideos y/o férula palmar nocturna en extensión que abarque mano y antebrazo. Si persisten los síntomas, puede realizarse una infiltración de corticoides, ya que existen evidencias que la inyección local de metil-prednisolona mejora los síntomas.  Está indicada la cirugía si persisten los síntomas a pesar del tratamiento médico, si el estudio electrofisiológico es muy patológico o si existe déficit sensitivo o motor establecido. La cirugía es eficaz en la mejoría del dolor con lenta o nula recuperación de déficit sensitivo y motor previos.  Palabras clave: Síndrome túnel carpiano. Nervio mediano. Neuropatía compresiva.  &nbsp

A History of Spike-Timing-Dependent Plasticity

How learning and memory is achieved in the brain is a central question in neuroscience. Key to today’s research into information storage in the brain is the concept of synaptic plasticity, a notion that has been heavily influenced by Hebb's (1949) postulate. Hebb conjectured that repeatedly and persistently co-active cells should increase connective strength among populations of interconnected neurons as a means of storing a memory trace, also known as an engram. Hebb certainly was not the first to make such a conjecture, as we show in this history. Nevertheless, literally thousands of studies into the classical frequency-dependent paradigm of cellular learning rules were directly inspired by the Hebbian postulate. But in more recent years, a novel concept in cellular learning has emerged, where temporal order instead of frequency is emphasized. This new learning paradigm – known as spike-timing-dependent plasticity (STDP) – has rapidly gained tremendous interest, perhaps because of its combination of elegant simplicity, biological plausibility, and computational power. But what are the roots of today’s STDP concept? Here, we discuss several centuries of diverse thinking, beginning with philosophers such as Aristotle, Locke, and Ribot, traversing, e.g., Lugaro’s plasticità and Rosenblatt’s perceptron, and culminating with the discovery of STDP. We highlight interactions between theoretical and experimental fields, showing how discoveries sometimes occurred in parallel, seemingly without much knowledge of the other field, and sometimes via concrete back-and-forth communication. We point out where the future directions may lie, which includes interneuron STDP, the functional impact of STDP, its mechanisms and its neuromodulatory regulation, and the linking of STDP to the developmental formation and continuous plasticity of neuronal networks

The Impact of Muscular Strength on Cardiovascular Disease Risk Factors

The purpose of this study was to determine the associations between isokinetic leg muscular strength and cardiovascular disease (CVD) risk factor characterizations in Americans aged 50 and older. Using a publicly available dataset from the National Health and Nutrition Examination Survey (NHANES), a secondary analysis was conducted on participants (males ≥50 yrs; females ≥55 yrs; N=10,858) pooled from 1999 to 2002. CVD risk factors were determined using the American College of Sports Medicine (ACSM) cutoff values. CVD risk factor characterization was determined by creating CVD risk factor profiles (i.e., the total number of CVD risk factors an individual possesses), then separating participants into low (0-2 CVD risk factors), moderate (3-5), and high (6-8) risk groups. Muscular strength was determined by isokinetic maximal peak force (PF) of the leg extensors, both raw and normalized to body mass. Normalized, but not raw, muscular strength was shown to be significantly inversely associated with CVD risk factor characterization for both males and females (Phttps://digitalcommons.odu.edu/gradposters2022_education/1002/thumbnail.jp

Non-equilibrium dynamics of stochastic point processes with refractoriness

Stochastic point processes with refractoriness appear frequently in the quantitative analysis of physical and biological systems, such as the generation of action potentials by nerve cells, the release and reuptake of vesicles at a synapse, and the counting of particles by detector devices. Here we present an extension of renewal theory to describe ensembles of point processes with time varying input. This is made possible by a representation in terms of occupation numbers of two states: Active and refractory. The dynamics of these occupation numbers follows a distributed delay differential equation. In particular, our theory enables us to uncover the effect of refractoriness on the time-dependent rate of an ensemble of encoding point processes in response to modulation of the input. We present exact solutions that demonstrate generic features, such as stochastic transients and oscillations in the step response as well as resonances, phase jumps and frequency doubling in the transfer of periodic signals. We show that a large class of renewal processes can indeed be regarded as special cases of the model we analyze. Hence our approach represents a widely applicable framework to define and analyze non-stationary renewal processes.Comment: 8 pages, 4 figure

Generalized Rate-Code Model for Neuron Ensembles with Finite Populations

We have proposed a generalized Langevin-type rate-code model subjected to multiplicative noise, in order to study stationary and dynamical properties of an ensemble containing {\it finite} $N$ neurons. Calculations using the Fokker-Planck equation (FPE) have shown that owing to the multiplicative noise, our rate model yields various kinds of stationary non-Gaussian distributions such as gamma, inverse-Gaussian-like and log-normal-like distributions, which have been experimentally observed. Dynamical properties of the rate model have been studied with the use of the augmented moment method (AMM), which was previously proposed by the author with a macroscopic point of view for finite-unit stochastic systems. In the AMM, original $N$-dimensional stochastic differential equations (DEs) are transformed into three-dimensional deterministic DEs for means and fluctuations of local and global variables. Dynamical responses of the neuron ensemble to pulse and sinusoidal inputs calculated by the AMM are in good agreement with those obtained by direct simulation. The synchronization in the neuronal ensemble is discussed. Variabilities of the firing rate and of the interspike interval (ISI) are shown to increase with increasing the magnitude of multiplicative noise, which may be a conceivable origin of the observed large variability in cortical neurons.Comment: 19 pages, 9 figures, accepted in Phys. Rev. E after minor modification

Comparison of Langevin and Markov channel noise models for neuronal signal generation

The stochastic opening and closing of voltage-gated ion channels produces noise in neurons. The effect of this noise on the neuronal performance has been modelled using either approximate or Langevin model, based on stochastic differential equations or an exact model, based on a Markov process model of channel gating. Yet whether the Langevin model accurately reproduces the channel noise produced by the Markov model remains unclear. Here we present a comparison between Langevin and Markov models of channel noise in neurons using single compartment Hodgkin-Huxley models containing either $Na^{+}$ and $K^{+}$, or only $K^{+}$ voltage-gated ion channels. The performance of the Langevin and Markov models was quantified over a range of stimulus statistics, membrane areas and channel numbers. We find that in comparison to the Markov model, the Langevin model underestimates the noise contributed by voltage-gated ion channels, overestimating information rates for both spiking and non-spiking membranes. Even with increasing numbers of channels the difference between the two models persists. This suggests that the Langevin model may not be suitable for accurately simulating channel noise in neurons, even in simulations with large numbers of ion channels