Sympathetic nervous system | EPFL Graph Search

The sympathetic nervous system (SNS) is one of the three divisions of the autonomic nervous system, the others being the parasympathetic nervous system and the enteric nervous system. The enteric nervous system is sometimes considered part of the autonomic nervous system, and sometimes considered an independent system. The autonomic nervous system functions to regulate the body's unconscious actions. The sympathetic nervous system's primary process is to stimulate the body's fight or flight response. It is, however, constantly active at a basic level to maintain homeostasis. The sympathetic nervous system is described as being antagonistic to the parasympathetic nervous system. The latter stimulates the body to "feed and breed" and to (then) "rest-and-digest". Structure There are two kinds of neurons involved in the transmission of any signal through the sympathetic system: pre-ganglionic and post-ganglionic. The shorter preganglionic neurons originate in the thoracolumbar

Electr(on)ic palpitations: a visitors' pavilion for the Bieudron power plant, Switzerland

Michael Jakob

The electric power system has often been compared to a circulatory system, and telecommunication and informational complexes likened to nervous systems. Such characterisations are rigorous only for those aspects that bring the utility system closer to a living system: its mechanisms of control and regulation. Copyright © Cambridge University Press 2010.

2010

The Neuron Phenotype Ontology: A FAIR Approach to Proposing and Classifying Neuronal Types

Sean Lewis Hill, Mohameth François Sy

The challenge of defining and cataloging the building blocks of the brain requires a standardized approach to naming neurons and organizing knowledge about their properties. The US Brain Initiative Cell Census Network, Human Cell Atlas, Blue Brain Project, and others are generating vast amounts of data and characterizing large numbers of neurons throughout the nervous system. The neuroscientific literature contains many neuron names (e.g. parvalbumin-positive interneuron or layer 5 pyramidal cell) that are commonly used and generally accepted. However, it is often unclear how such common usage types relate to many evidence-based types that are proposed based on the results of new techniques. Further, comparing different types across labs remains a significant challenge. Here, we propose an interoperable knowledge representation, the Neuron Phenotype Ontology (NPO), that provides a standardized and automatable approach for naming cell types and normalizing their constituent phenotypes using identifiers from community ontologies as a common language. The NPO provides a framework for systematically organizing knowledge about cellular properties and enables interoperability with existing neuron naming schemes. We evaluate the NPO by populating a knowledge base with three independent cortical neuron classifications derived from published data sets that describe neurons according to molecular, morphological, electrophysiological, and synaptic properties. Competency queries to this knowledge base demonstrate that the NPO knowledge model enables interoperability between the three test cases and neuron names commonly used in the literature.

HUMANA PRESS INC2022

Post-translational regulation of neuronal differentiation

Jaipreet Singh Loomba

Glycosphingolipids (GSLs) are amphipathic lipid moieties that make up only 3% of the total lipid content of the cell and are almost exclusively expressed at the Plasma Membrane(PM). They are key drivers of signalling hotspots known as âlipid-raftsâ as well as acting as primary signalling molecules themselves. Pathologically, perturbations in their synthesis (Knock-Out mice models) and disorders in their metabolism(Lysosomal storage disorders), both converge on neurological symptoms. In fact, during neuronal development, stem cells have been known to completely remodel their glycosphingolipid profiles, so much so, that the developmental stages of the nervous system have been associated with the expression of different glycosphingolipids. This coordinated change in the expression of glycosphingolipids has been previously attributed to the transcriptional shift in the the expression of genes encoding specific Glycosphingolipid Synthesizing Enzymes (GSEs) observed over neuronal development and, more recently, shown to be internally regulated by the GSLs themselves whereby globosides negatively regulate the expression of the ganglioside synthesizing enzyme GM3S via a neuronal transcription factor AUTS2. In this thesis I show that there exists an extra layer of post-translational regulation that is active over neuronal development that destabilizes the Gb3 synthesizing enzyme, Gb3S, on one hand while stabilizing the GM3S on the other. The regulatory mechanism achieves this effect by doubling the rate of degradation of Gb3S in neuronal cells, probably via membrane trafficking events. The exact details of the stabilization effect of GM3S remains to be determined as the results could not ascertain if it was the same mechanism or a completely different one. My study goes on to show that this regulatory mechanism is activated early during development, preceding the changes in canonical stem and neuronal markers. Morphologically, the study points towards a post-compaction but pre-cavitation (E2.5-E3.5) point of activation for the mechanism of Gb3S destabalization, relative to early mouse embryological development. Furthermore, I found that the Gb3S interactor and AUTS2 transcriptional target UCHL1 is a key regulatory unit of the machinery such that inhibiting its activity results in a specific rescue of the Gb3S enzyme.

EPFL2021

Post-translational regulation of neuronal differentiation

Jaipreet Singh Loomba

EPFL2021