A cortical network underpinning the perceptual priority for rising intensity and auditory ‘‘looming.’’

2002 ◽  
Vol 111 (5) ◽  
pp. 2355
Author(s):  
John G. Neuhoff ◽  
Deniz Bilecen ◽  
Henrietta Mustovic ◽  
Hartmut Schachinger ◽  
Erich Seifritz ◽  
...  

2014 ◽  
Vol 1 ◽  
pp. 563-565
Author(s):  
M.V. Sanchez-Vives ◽  
Maurizio Mattia


PLoS ONE ◽  
2019 ◽  
Vol 14 (7) ◽  
pp. e0218529 ◽  
Author(s):  
Elizabeth A. Bock ◽  
Jeremy D. Fesi ◽  
Sylvain Baillet ◽  
Janine D. Mendola


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Zhong Li ◽  
Jin-Xing Wei ◽  
Guang-Wei Zhang ◽  
Junxiang J. Huang ◽  
Brian Zingg ◽  
...  

AbstractAnimals exhibit innate defense behaviors in response to approaching threats cued by the dynamics of sensory inputs of various modalities. The underlying neural circuits have been mostly studied in the visual system, but remain unclear for other modalities. Here, by utilizing sounds with increasing (vs. decreasing) loudness to mimic looming (vs. receding) objects, we find that looming sounds elicit stereotypical sequential defensive reactions: freezing followed by flight. Both behaviors require the activity of auditory cortex, in particular the sustained type of responses, but are differentially mediated by corticostriatal projections primarily innervating D2 neurons in the tail of the striatum and corticocollicular projections to the superior colliculus, respectively. The behavioral transition from freezing to flight can be attributed to the differential temporal dynamics of the striatal and collicular neurons in their responses to looming sound stimuli. Our results reveal an essential role of the striatum in the innate defense control.



2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Emma M. Perkins ◽  
Karen Burr ◽  
Poulomi Banerjee ◽  
Arpan R. Mehta ◽  
Owen Dando ◽  
...  

Abstract Background Physiological disturbances in cortical network excitability and plasticity are established and widespread in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) patients, including those harbouring the C9ORF72 repeat expansion (C9ORF72RE) mutation – the most common genetic impairment causal to ALS and FTD. Noting that perturbations in cortical function are evidenced pre-symptomatically, and that the cortex is associated with widespread pathology, cortical dysfunction is thought to be an early driver of neurodegenerative disease progression. However, our understanding of how altered network function manifests at the cellular and molecular level is not clear. Methods To address this we have generated cortical neurons from patient-derived iPSCs harbouring C9ORF72RE mutations, as well as from their isogenic expansion-corrected controls. We have established a model of network activity in these neurons using multi-electrode array electrophysiology. We have then mechanistically examined the physiological processes underpinning network dysfunction using a combination of patch-clamp electrophysiology, immunocytochemistry, pharmacology and transcriptomic profiling. Results We find that C9ORF72RE causes elevated network burst activity, associated with enhanced synaptic input, yet lower burst duration, attributable to impaired pre-synaptic vesicle dynamics. We also show that the C9ORF72RE is associated with impaired synaptic plasticity. Moreover, RNA-seq analysis revealed dysregulated molecular pathways impacting on synaptic function. All molecular, cellular and network deficits are rescued by CRISPR/Cas9 correction of C9ORF72RE. Our study provides a mechanistic view of the early dysregulated processes that underpin cortical network dysfunction in ALS-FTD. Conclusion These findings suggest synaptic pathophysiology is widespread in ALS-FTD and has an early and fundamental role in driving altered network function that is thought to contribute to neurodegenerative processes in these patients. The overall importance is the identification of previously unidentified defects in pre and postsynaptic compartments affecting synaptic plasticity, synaptic vesicle stores, and network propagation, which directly impact upon cortical function.





2021 ◽  
Vol 168 ◽  
pp. S196
Author(s):  
Xiaopeng Si ◽  
Shaoxin Xiang ◽  
Ludan Zhang ◽  
Sicheng Li ◽  
Kuo Zhang ◽  
...  


2012 ◽  
Vol 32 (6) ◽  
pp. 1918-1919 ◽  
Author(s):  
J. Seubert ◽  
K. Ohla


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