Neuronal Synchronization Can Control the Energy Efficiency of Inter-Spike Interval Coding

The role of synchronous firing in sensory coding and cognition remains controversial. While studies, focusing on its mechanistic consequences in attentional tasks, suggest that synchronization dynamically boosts sensory processing, others failed to find significant synchronization levels in such tasks. We attempt to understand both lines of evidence within a coherent theoretical framework. We conceptualize synchronization as an independent control parameter to study how the postsynaptic neuron transmits the average firing activity of a presynaptic population, in the presence of synchronization. We apply the Berger-Levy theory of energy efficient information transmission to interpret simulations of a Hodgkin-Huxley-type postsynaptic neuron model, where we varied the firing rate and synchronization level in the presynaptic population independently. We find that for a fixed presynaptic firing rate the simulated postsynaptic interspike interval distribution depends on the synchronization level and is well-described by a generalized extreme value distribution. For synchronization levels of 15% to 50%, we find that the optimal distribution of presynaptic firing rate, maximizing the mutual information per unit cost, is maximized at ~30% synchronization level. These results suggest that the statistics and energy efficiency of neuronal communication channels, through which the input rate is communicated, can be dynamically adapted by the synchronization level.Comment: 47 pages, 14 figures, 2 Table

Modulation of the GABAergic pathway for the treatment of fragile X syndrome.

Fragile X syndrome (FXS) is the most common genetic cause of intellectual disability and the most common single-gene cause of autism. It is caused by mutations on the fragile X mental retardation gene (FMR1) and lack of fragile X mental retardation protein, which in turn, leads to decreased inhibition of translation of many synaptic proteins. The metabotropic glutamate receptor (mGluR) hypothesis states that the neurological deficits in individuals with FXS are due mainly to downstream consequences of overstimulation of the mGluR pathway. The main efforts have focused on mGluR5 targeted treatments; however, investigation on the gamma-aminobutyric acid (GABA) system and its potential as a targeted treatment is less emphasized. The fragile X mouse models (Fmr1-knock out) show decreased GABA subunit receptors, decreased synthesis of GABA, increased catabolism of GABA, and overall decreased GABAergic input in many regions of the brain. Consequences of the reduced GABAergic input in FXS include oversensitivity to sensory stimuli, seizures, and anxiety. Deficits in the GABA receptors in different regions of the brain are associated with behavioral and attentional processing deficits linked to anxiety and autistic behaviors. The understanding of the neurobiology of FXS has led to the development of targeted treatments for the core behavioral features of FXS, which include social deficits, inattention, and anxiety. These symptoms are also observed in individuals with autism and other neurodevelopmental disorders, therefore the targeted treatments for FXS are leading the way in the treatment of other neurodevelopmental syndromes and autism. The GABAergic system in FXS represents a target for new treatments. Herein, we discuss the animal and human trials of GABAergic treatment in FXS. Arbaclofen and ganaxolone have been used in individuals with FXS. Other potential GABAergic treatments, such as riluzole, gaboxadol, tiagabine, and vigabatrin, will be also discussed. Further studies are needed to determine the safety and efficacy of GABAergic treatments for FXS

Sum rate analysis of multiple-access neuro-spike communication channel with dynamic spiking threshold

© 2019 Elsevier B.V. The information from outside world is encoded into spikes by the sensory neurons. These spikes are further propagated to different brain regions through various neural pathways. In the cortical region, each neuron receives inputs from multiple neurons that change its membrane potential. If the accumulated change in the membrane potential is more than a threshold value, a spike is generated. According to various studies in neuroscience, this spiking threshold adapts with time depending on the previous spike. This causes short-term changes in the neural responses giving rise to short-term plasticity. Therefore, in this paper, we analyze a multiple-input single-output (MISO) neuro-spike communication channel and study the effects of dynamic spiking threshold on mutual information and maximum achievable sum rate of the channel. Since spike generation consumes a generous portion of the metabolic energy provided to the brain, we further put metabolic constraint in calculating the mutual information and find a trade-off between maximum achievable sum rate and metabolic energy consumed. Moreover, we analyze three types of neurons present in the cortical region, i.e., Regular spiking, Intrinsic bursting and Fast spiking neurons. We aim to characterize these neurons in terms of encoding/transmission rates and energy expenditure. It will provide a guideline for the practical implementation of bio-inspired nanonetworks as well as for the development of ICT-based diagnosis and treatment techniques for neural diseases.This work was supported in part by European Research Council (ERC) under grant ERC-2013-CoG 616922 (Project MINERVA) and ERC-2017-PoC 780645 (ERC Proof of Concept project MINRGRACE)

Fundamentals of molecular information and communication science

© 1963-2012 IEEE. Molecular communication (MC) is the most promising communication paradigm for nanonetwork realization since it is a natural phenomenon observed among living entities with nanoscale components. Since MC significantly differs from classical communication systems, it mandates reinvestigation of information and communication theoretical fundamentals. The closest examples of MC architectures are present inside our own body. Therefore, in this paper, we investigate the existing literature on intrabody nanonetworks and different MC paradigms to establish and introduce the fundamentals of molecular information and communication science. We highlight future research directions and open issues that need to be addressed for revealing the fundamental limits of this science. Although the scope of this development encompasses wide range of applications, we particularly emphasize its significance for life sciences by introducing potential diagnosis and treatment techniques for diseases caused by dysfunction of intrabody nanonetworks

Why are probabilistic laws governing quantum mechanics and neurobiology?

We address the question: Why are dynamical laws governing in quantum mechanics and in neuroscience of probabilistic nature instead of being deterministic? We discuss some ideas showing that the probabilistic option offers advantages over the deterministic one.Comment: 40 pages, 8 fig

Redox Homeostasis in Neural Plasticity and the Aged Brain

Currently, humans can easily live for 60 years and more. This increase in life expectancy produces myriad changes in our bodies that diminish the individual’s physical and mental capacities and affect as well the functional capacity of individuals to interact appropriately with their social and physical environments. The oxidative theory of aging predicts an accumulation of oxidative damage to proteins, lipids, and DNA with age; as a consequence, the aged brain gradually suffers loss in neuronal functions, increasing the risk of developing neurodegenerative diseases and cognitive impairment. To date, there are no effective treatments to prevent age-related cognitive decline, making it urgent to identify the neural mechanisms that are altered during aging. In this chapter, we discuss the mechanisms that underlie synaptic plasticity, emphasizing the relationship between redox balance and neuronal function, and we also address current evidence supporting oxidative stress as an important contributing factor in brain aging

PACAP and migraine headache: immunomodulation of neural circuits in autonomic ganglia and brain parenchyma.

The discovery that intravenous (IV) infusions of the neuropeptide PACAP-38 (pituitary adenylyl cyclase activating peptide-38) induced delayed migraine-like headaches in a large majority of migraine patients has resulted in considerable excitement in headache research. In addition to suggesting potential therapeutic targets for migraine, the finding provides an opportunity to better understand the pathological events from early events (aura) to the headache itself. Although PACAP-38 and the closely related peptide VIP (vasoactive intestinal peptide) are well-known as vasoactive molecules, the dilation of cranial blood vessels per se is no longer felt to underlie migraine headaches. Thus, more recent research has focused on other possible PACAP-mediated mechanisms, and has raised some important questions. For example, (1) are endogenous sources of PACAP (or VIP) involved in the triggering and/or propagation of migraine headaches?; (2) which receptor subtypes are involved in migraine pathophysiology?; (3) can we identify specific anatomical circuit(s) where PACAP signaling is involved in the features of migraine? The purpose of this review is to discuss the possibility, and supportive evidence, that PACAP acts to induce migraine-like symptoms not only by directly modulating nociceptive neural circuits, but also by indirectly regulating the production of inflammatory mediators. We focus here primarily on postulated extra-dural sites because potential mechanisms of PACAP action in the dura are discussed in detail elsewhere (see X, this edition)

Sum Rate of MISO Neuro-Spike Communication Channel With Constant Spiking Threshold.

Communication among neurons, known as neuro-spike communication, is the most promising technique for realization of a bio-inspired nanoscale communication paradigm to achieve biocompatible nanonetworks. In neuro-spike communication, the information, encoded into spike trains, is communicated to various brain regions through neuronal network. An output neuron needs to receive signal from multiple input neurons to generate a spike. Hence, in this paper, we aim to quantify the information transmitted through the multiple-input single-output (MISO) neuro-spike communication channel by considering models for axonal propagation, synaptic transmission, and spike generation. Moreover, the spike generation and propagation in each neuron requires opening and closing of numerous ionic channels on the cell membrane, which consumes considerable amount of ATP molecules called metabolic energy. Thus, we evaluate how applying a constraint on available metabolic energy affects the maximum achievable mutual information of this system. To this aim, we derive a closed form equation for the sum rate of the MISO neuro-spike communication channel and analyze it under the metabolic cost constraints. Finally, we discuss the impacts of changes in number of pre-synaptic neurons on the achievable rate and quantify the tradeoff between maximum achievable sum rate and the consumed metabolic energy

Perspectives on the Neuroscience of Cognition and Consciousness

The origin and current use of the concepts of computation, representation and information in Neuroscience are examined and conceptual flaws are identified which vitiate their usefulness for addressing problems of the neural basis of Cognition and Consciousness. In contrast, a convergence of views is presented to support the characterization of the Nervous System as a complex dynamical system operating in the metastable regime, and capable of evolving to configurations and transitions in phase space with potential relevance for Cognition and Consciousness