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"Neural circuitry"
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Principles of neural design
In this work, Peter Sterling and Simon Laughlin, two leading neuroscientists, outline a set of organizing principles to explain the whys of neural design that allow the brain to compute so efficiently. Setting out to 'reverse engineer' the brain - disassembling it to understand it - Sterling and Laughlin first consider why an animal should need a brain, tracing computational abilities from bacterium to protozoan to worm.
Book
Principles of Neural Design
Neuroscience research has exploded, with more than fifty thousand neuroscientists applying increasingly advanced methods. A mountain of new facts and mechanisms has emerged. And yet a principled framework to organize this knowledge has been missing. In this book, Peter Sterling and Simon Laughlin, two leading neuroscientists, strive to fill this gap, outlining a set of organizing principles to explain the whys of neural design that allow the brain to compute so efficiently. Setting out to \"reverse engineer\" the brain -- disassembling it to understand it -- Sterling and Laughlin first consider why an animal should need a brain, tracing computational abilities from bacterium to protozoan to worm. They examine bigger brains and the advantages of \"anticipatory regulation\"; identify constraints on neural design and the need to \"nanofy\"; and demonstrate the routes to efficiency in an integrated molecular system, phototransduction. They show that the principles of neural design at finer scales and lower levels apply at larger scales and higher levels; describe neural wiring efficiency; and discuss learning as a principle of biological design that includes \"save only what is needed.\"Sterling and Laughlin avoid speculation about how the brainmightwork and endeavor to make sense of what is already known. Their distinctive contribution is to gather a coherent set of basic rules and exemplify them across spatial and functional scales.
eBook
RibosomeRelA structures reveal the mechanism of stringent response activation
Stringent response is a conserved bacterial stress response underlying virulence and antibiotic resistance. RelA/SpoT-homolog proteins synthesize transcriptional modulators (p)ppGpp, allowing bacteria to adapt to stress. RelA is activated during amino-acid starvation, when cognate deacyl-tRNA binds to the ribosomal A (aminoacyl-tRNA) site. We report four cryo-EM structures of E. coli RelA bound to the 70S ribosome, in the absence and presence of deacyl-tRNA accommodating in the 30S A site. The boomerang-shaped RelA with a wingspan of more than 100 Å wraps around the A/R (30S A-site/RelA-bound) tRNA. The CCA end of the A/R tRNA pins the central TGS domain against the 30S subunit, presenting the (p)ppGpp-synthetase domain near the 30S spur. The ribosome and A/R tRNA are captured in three conformations, revealing hitherto elusive states of tRNA engagement with the ribosomal decoding center. Decoding-center rearrangements are coupled with the step-wise 30S-subunit 'closure', providing insights into the dynamics of high-fidelity tRNA decoding.
Journal Article
The medial septum-hippocampus-lateral septum circuitry in spatial memory: linking healthy function to early Alzheimer’s disease and translational opportunities
Hippocampus (HPC)-associated spatial memory deficits are one of the earliest symptoms of Alzheimer’s disease (AD). Current pharmacological treatments only alleviate the symptoms but do not prevent disease progression. The emergence of neuromodulation technology suggests that specific neural circuits are potential therapeutic targets for AD. Current studies have analyzed the medial septum (MS)–HPC and the HPC–lateral septum (LS) circuitries separately. A comprehensive understanding of their synergistic effects and overall dysregulation in AD remains limited. In this review, we will integrate anatomical and functional evidence to give an overview of the role of the MS–HPC–LS circuitry in spatial memory, the mechanisms of AD-related dysregulation, and therapeutic strategies targeting the circuitry, specially focusing on molecular interventions (receptor modulation) and bioengineering strategies (circuit-specific stimulation).
Journal Article
GABA.sub.BR silencing of nerve terminals
Control of neurotransmission efficacy is central to theories of how the brain computes and stores information. Presynaptic G-protein coupled receptors (GPCRs) are critical in this problem as they locally influence synaptic strength and can operate on a wide range of time scales. Among the mechanisms by which GPCRs impact neurotransmission is by inhibiting voltage-gated calcium (Ca.sup.2+) influx in the active zone. Here, using quantitative analysis of both single bouton Ca.sup.2+ influx and exocytosis, we uncovered an unexpected non-linear relationship between the magnitude of action potential driven Ca.sup.2+ influx and the concentration of external Ca.sup.2+ ([Ca.sup.2+].sub.e). We find that this unexpected relationship is leveraged by GPCR signaling when operating at the nominal physiological set point for [Ca.sup.2+].sub.e, 1.2 mM, to achieve complete silencing of nerve terminals. These data imply that the information throughput in neural circuits can be readily modulated in an all-or-none fashion at the single synapse level when operating at the physiological set point.
Journal Article
Speech synthesis from neural decoding of spoken sentences
Technology that translates neural activity into speech would be transformative for people who are unable to communicate as a result of neurological impairments. Decoding speech from neural activity is challenging because speaking requires very precise and rapid multi-dimensional control of vocal tract articulators. Here we designed a neural decoder that explicitly leverages kinematic and sound representations encoded in human cortical activity to synthesize audible speech. Recurrent neural networks first decoded directly recorded cortical activity into representations of articulatory movement, and then transformed these representations into speech acoustics. In closed vocabulary tests, listeners could readily identify and transcribe speech synthesized from cortical activity. Intermediate articulatory dynamics enhanced performance even with limited data. Decoded articulatory representations were highly conserved across speakers, enabling a component of the decoder to be transferrable across participants. Furthermore, the decoder could synthesize speech when a participant silently mimed sentences. These findings advance the clinical viability of using speech neuroprosthetic technology to restore spoken communication.
A neural decoder uses kinematic and sound representations encoded in human cortical activity to synthesize audible sentences, which are readily identified and transcribed by listeners.
Journal Article
Hierarchical organization of cortical and thalamic connectivity
The mammalian cortex is a laminar structure containing many areas and cell types that are densely interconnected in complex ways, and for which generalizable principles of organization remain mostly unknown. Here we describe a major expansion of the Allen Mouse Brain Connectivity Atlas resource
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, involving around a thousand new tracer experiments in the cortex and its main satellite structure, the thalamus. We used Cre driver lines (mice expressing Cre recombinase) to comprehensively and selectively label brain-wide connections by layer and class of projection neuron. Through observations of axon termination patterns, we have derived a set of generalized anatomical rules to describe corticocortical, thalamocortical and corticothalamic projections. We have built a model to assign connection patterns between areas as either feedforward or feedback, and generated testable predictions of hierarchical positions for individual cortical and thalamic areas and for cortical network modules. Our results show that cell-class-specific connections are organized in a shallow hierarchy within the mouse corticothalamic network.
Using mouse lines in which subsets of neurons are genetically labelled, the authors provide generalized anatomical rules for connections within and between the cortex and thalamus.
Journal Article