Neural network activity and neurological soft signs in healthy adults

2015 ◽  
Vol 278 ◽  
pp. 514-519 ◽  
Author(s):  
Philipp A. Thomann ◽  
Dusan Hirjak ◽  
Katharina M. Kubera ◽  
Bram Stieltjes ◽  
Robert C. Wolf
2019 ◽  
Vol 709 ◽  
pp. 134398
Author(s):  
Nifareeda Samerphob ◽  
Acharaporn Issuriya ◽  
Dania Cheaha ◽  
Surapong Chatpun ◽  
Ole Jensen ◽  
...  

Neuroscience ◽  
2020 ◽  
Vol 446 ◽  
pp. 171-198 ◽  
Author(s):  
Philip A. Adeniyi ◽  
Amita Shrestha ◽  
Olalekan M. Ogundele

1997 ◽  
Vol 110 (3-4) ◽  
pp. 323-331 ◽  
Author(s):  
L. Menendez de la Prida ◽  
N. Stollenwerk ◽  
J.V. Sanchez-Andres

2017 ◽  
Vol 60 ◽  
pp. 280-292 ◽  
Author(s):  
Andrea Vassallo ◽  
Michela Chiappalone ◽  
Ricardo De Camargos Lopes ◽  
Bibiana Scelfo ◽  
Antonio Novellino ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Francesco Ferrini ◽  
Yves De Koninck

Microglia-neuron interactions play a crucial role in several neurological disorders characterized by altered neural network excitability, such as epilepsy and neuropathic pain. While a series of potential messengers have been postulated as substrates of the communication between microglia and neurons, including cytokines, purines, prostaglandins, and nitric oxide, the specific links between messengers, microglia, neuronal networks, and diseases have remained elusive. Brain-derived neurotrophic factor (BDNF) released by microglia emerges as an exception in this riddle. Here, we review the current knowledge on the role played by microglial BDNF in controlling neuronal excitability by causing disinhibition. The efforts made by different laboratories during the last decade have collectively provided a robust mechanistic paradigm which elucidates the mechanisms involved in the synthesis and release of BDNF from microglia, the downstream TrkB-mediated signals in neurons, and the biophysical mechanism by which disinhibition occurs, via the downregulation of the K+-Cl−cotransporter KCC2, dysrupting Cl−homeostasis, and hence the strength ofGABAA- and glycine receptor-mediated inhibition. The resulting altered network activity appears to explain several features of the associated pathologies. Targeting the molecular players involved in this canonical signaling pathway may lead to novel therapeutic approach for ameliorating a wide array of neural dysfunctions.


2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Mürsel Karadas ◽  
Adam M. Wojciechowski ◽  
Alexander Huck ◽  
Nils Ole Dalby ◽  
Ulrik Lund Andersen ◽  
...  

2004 ◽  
Vol 15 (6) ◽  
pp. 796-801 ◽  
Author(s):  
Chihiro Yokoyama ◽  
Hideo Tsukada ◽  
Yasuyoshi Watanabe ◽  
Hirotaka Onoe

Author(s):  
Davide Valeriani ◽  
Kristina Simonyan

Speech production relies on the orchestrated control of multiple brain regions. The specific, directional influences within these networks remain poorly understood. We used regression dynamic causal modelling to infer the whole-brain directed (effective) connectivity from functional magnetic resonance imaging data of 36 healthy individuals during the production of meaningful English sentences and meaningless syllables. We identified that the two dynamic connectomes have distinct architectures that are dependent on the complexity of task production. The speech was regulated by a dynamic neural network, the most influential nodes of which were centred around superior and inferior parietal areas and influenced the whole-brain network activity via long-ranging coupling with primary sensorimotor, prefrontal, temporal and insular regions. By contrast, syllable production was controlled by a more compressed, cost-efficient network structure, involving sensorimotor cortico-subcortical integration via superior parietal and cerebellar network hubs. These data demonstrate the mechanisms by which the neural network reorganizes the connectivity of its influential regions, from supporting the fundamental aspects of simple syllabic vocal motor output to multimodal information processing of speech motor output. This article is part of the theme issue ‘Vocal learning in animals and humans’.


2019 ◽  
Author(s):  
Ranmal A. Samarasinghe ◽  
Osvaldo A. Miranda ◽  
Simon Mitchell ◽  
Isabella Ferando ◽  
Momoko Watanabe ◽  
...  

ABSTRACTHuman brain organoids represent a powerful tool for the study of human neurological diseases particularly those that impact brain growth and structure. However, many neurological diseases lack obvious anatomical abnormalities, yet significantly impact neural network functions, raising the question of whether organoids possess sufficient neural network architecture and complexity to model these conditions. Here, we explore the network level functions of brain organoids using calcium sensor imaging and extracellular recording approaches that together reveal the existence of complex oscillatory network behaviors reminiscent of intact brain preparations. We further demonstrate strikingly abnormal epileptiform network activity in organoids derived from a Rett Syndrome patient despite only modest anatomical differences from isogenically matched controls, and rescue with an unconventional neuromodulatory drug Pifithrin-α. Together, these findings provide an essential foundation for the utilization of human brain organoids to study intact and disordered human brain network formation and illustrate their utility in therapeutic discovery.


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