Advances in Clinical Neurophysiology

Including some of the newest advances in the field of neurophysiology, this book can be considered as one of the treasures that interested scientists would like to collect. It discusses many disciplines of clinical neurophysiology that are, currently, crucial in the practice as they explain methods and findings of techniques that help to improve diagnosis and to ensure better treatment. While trying to rely on evidence-based facts, this book presents some new ideas to be applied and tested in the clinical practice. Advances in Clinical Neurophysiology is important not only for the neurophysiologists but also for clinicians interested or working in wide range of specialties such as neurology, neurosurgery, intensive care units, pediatrics and so on. Generally, this book is written and designed to all those involved in, interpreting or requesting neurophysiologic tests

Perspectives on adaptive dynamical systems

Adaptivity is a dynamical feature that is omnipresent in nature, socio-economics, and technology. For example, adaptive couplings appear in various real-world systems like the power grid, social, and neural networks, and they form the backbone of closed-loop control strategies and machine learning algorithms. In this article, we provide an interdisciplinary perspective on adaptive systems. We reflect on the notion and terminology of adaptivity in different disciplines and discuss which role adaptivity plays for various fields. We highlight common open challenges, and give perspectives on future research directions, looking to inspire interdisciplinary approaches.Comment: 46 pages, 9 figure

Exploring the Role of PANNEXIN1A in an Acute Experimental Model of Parkinson's Disease

In the nervous system Pannexin1 channels are major ATP and glutamate release sites. The channels are implicated in neurodegenerative disorders including Parkinson’s disease, but the underlying mechanisms remain unclear. Here, an interdisciplinary approach tested roles of the mammalian Pannexin1 ortholog Pannexin1a in a zebrafish model of MPTP-induced early stages of Parkinson’s disease at molecular, systems, and behavioral levels. The short-term treatment of wild-type TL and gene-edited Panx1a-KO larvae caused metabolic stress, regulated inflammatory pathways, and reduced ATP production. Local field potentials recorded from three regions of the ascending visual pathway showed complex changes in the beta- and gamma-band power and in the coherence between these regions. MPTP treatment produced significantly impaired movements which were partially rescued by targeting the NLRP3 inflammasome. The main findings of this research provide evidence that Panx1a serves a neuroprotective role in an acute MPTP model of Parkinson's disease

Exploring the Role of PANNEXIN1A in an Acute Experimental Model of Parkinson's Disease

In the nervous system Pannexin1 channels are major ATP and glutamate release sites. The channels are implicated in neurodegenerative disorders including Parkinsons disease, but the underlying mechanisms remain unclear. Here, an interdisciplinary approach tested roles of the mammalian Pannexin1 ortholog Pannexin1a in a zebrafish model of MPTP-induced early stages of Parkinsons disease at molecular, systems, and behavioral levels. The short-term treatment of wild-type TL and gene-edited Panx1a-KO larvae caused metabolic stress, regulated inflammatory pathways, and reduced ATP production. Local field potentials recorded from three regions of the ascending visual pathway showed complex changes in the beta- and gamma-band power and in the coherence between these regions. MPTP treatment produced significantly impaired movements which were partially rescued by targeting the NLRP3 inflammasome. The main findings of this research provide evidence that Panx1a serves a neuroprotective role in an acute MPTP model of Parkinson's disease

25th Annual Computational Neuroscience Meeting: CNS-2016

Abstracts of the 25th Annual Computational Neuroscience Meeting: CNS-2016 Seogwipo City, Jeju-do, South Korea. 2–7 July 201

25th annual computational neuroscience meeting: CNS-2016

The same neuron may play different functional roles in the neural circuits to which it belongs. For example, neurons in the Tritonia pedal ganglia may participate in variable phases of the swim motor rhythms [1]. While such neuronal functional variability is likely to play a major role the delivery of the functionality of neural systems, it is difficult to study it in most nervous systems. We work on the pyloric rhythm network of the crustacean stomatogastric ganglion (STG) [2]. Typically network models of the STG treat neurons of the same functional type as a single model neuron (e.g. PD neurons), assuming the same conductance parameters for these neurons and implying their synchronous firing [3, 4]. However, simultaneous recording of PD neurons shows differences between the timings of spikes of these neurons. This may indicate functional variability of these neurons. Here we modelled separately the two PD neurons of the STG in a multi-neuron model of the pyloric network. Our neuron models comply with known correlations between conductance parameters of ionic currents. Our results reproduce the experimental finding of increasing spike time distance between spikes originating from the two model PD neurons during their synchronised burst phase. The PD neuron with the larger calcium conductance generates its spikes before the other PD neuron. Larger potassium conductance values in the follower neuron imply longer delays between spikes, see Fig. 17.Neuromodulators change the conductance parameters of neurons and maintain the ratios of these parameters [5]. Our results show that such changes may shift the individual contribution of two PD neurons to the PD-phase of the pyloric rhythm altering their functionality within this rhythm. Our work paves the way towards an accessible experimental and computational framework for the analysis of the mechanisms and impact of functional variability of neurons within the neural circuits to which they belong

A Drosophila model of generalised epilepsy and paroxysmal dyskinesia: generation, characterisation, and functional analysis

Generalised epilepsy and paroxysmal dyskinesia (GEPD) patients present with epilepsy (absence- and generalised tonic-clonic seizures), paroxysmal dyskinesia (non-kinesigenic), or a combination thereof. GEPD is linked to a missense mutation (D434G) in KCNMA1, which encodes the alpha-subunit of the BK channel, a Ca2+- and voltage-activated K+ channel. Previous studies have demonstrated that this mutation causes a gain of BK channel function by potentiating the allosteric coupling between Ca2+ binding and channel opening. Due to the role of BK channels in action potential repolarisation, it has been hypothesised that the D434G mutation narrows action potential width and increases neuronal firing frequencies, leading to seizures and dyskinetic attacks. // However, BK channels are expressed broadly throughout the human body, including various extra-neuronal tissues, and, on a subcellular level, localise not only to the plasma membrane but also to various intracellular organelles. Due to this pleiotropy, the organismal effects of the D434G mutation remain unclear. In this thesis, I present the generation, characterisation, and functional analysis of a novel knock-in fly model carrying the D434G-equivalent E366G mutation in slowpoke (slo), the Drosophila orthologue of KCNMA1 – this novel slo allele is termed sloE366G. // Evidence is provided that the E366G mutation increases the Ca2+-sensitivity of Slo channels ex vivo. Moreover, sloE366G/+ animals exhibit a severe decrease in locomotion and altered action selection, phenotypes that correlate with aberrant motoneuron activity, as shown via electrophysiology and live optical imaging. Using a genetic approach, I demonstrate that cholinergic neurons mediate this locomotor defect. Further, via RNA-sequencing I provide evidence that sloE366G/+ flies exhibit altered metabolic-, redox-, and immune function, and that the stress-responsive transcription factor foxo genetically interacts with sloE366G. Together, these data suggest a pathogenic locus for GEPD and define molecular pathways involved in GEPD pathogenesis

Programming the cerebellum

It is argued that large-scale neural network simulations of cerebellar cortex and nuclei, based on realistic compartmental models of me major cell populations, are necessary before the problem of motor learning in the cerebellum can be solved, [HOUK et al.; SIMPSON et al.