scholarly journals Author response: Developmental loss of MeCP2 from VIP interneurons impairs cortical function and behavior

Author(s):  
James M Mossner ◽  
Renata Batista-Brito ◽  
Rima Pant ◽  
Jessica A Cardin
2020 ◽  
Author(s):  
Emily A Bayer ◽  
Rebecca C Stecky ◽  
Lauren Neal ◽  
Phinikoula S Katsamba ◽  
Goran Ahlsen ◽  
...  

2016 ◽  
Vol 113 (27) ◽  
pp. 7337-7344 ◽  
Author(s):  
Michael Hawrylycz ◽  
Costas Anastassiou ◽  
Anton Arkhipov ◽  
Jim Berg ◽  
Michael Buice ◽  
...  

The scientific mission of the Project MindScope is to understand neocortex, the part of the mammalian brain that gives rise to perception, memory, intelligence, and consciousness. We seek to quantitatively evaluate the hypothesis that neocortex is a relatively homogeneous tissue, with smaller functional modules that perform a common computational function replicated across regions. We here focus on the mouse as a mammalian model organism with genetics, physiology, and behavior that can be readily studied and manipulated in the laboratory. We seek to describe the operation of cortical circuitry at the computational level by comprehensively cataloging and characterizing its cellular building blocks along with their dynamics and their cell type-specific connectivities. The project is also building large-scale experimental platforms (i.e., brain observatories) to record the activity of large populations of cortical neurons in behaving mice subject to visual stimuli. A primary goal is to understand the series of operations from visual input in the retina to behavior by observing and modeling the physical transformations of signals in the corticothalamic system. We here focus on the contribution that computer modeling and theory make to this long-term effort.


2018 ◽  
Author(s):  
Anissa Bara ◽  
Antonia Manduca ◽  
Axel Bernabeu ◽  
Milene Borsoi ◽  
Michela Serviado ◽  
...  

2020 ◽  
Author(s):  
Joanna Weidler‐Lewis ◽  
Michelle Wooten ◽  
Scott P. McDonald
Keyword(s):  

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
James M Mossner ◽  
Renata Batista-Brito ◽  
Rima Pant ◽  
Jessica A Cardin

Rett Syndrome is a devastating neurodevelopmental disorder resulting from mutations in the gene MECP2. Mutations of Mecp2 that are restricted to GABAergic cell types largely replicate the behavioral phenotypes associated with mouse models of Rett Syndrome, suggesting a pathophysiological role for inhibitory interneurons. Recent work has suggested that vasoactive intestinal peptide-expressing (VIP) interneurons may play a critical role in the proper development and function of cortical circuits, making them a potential key point of vulnerability in neurodevelopmental disorders. However, little is known about the role of VIP interneurons in Rett Syndrome. Here we find that loss of MeCP2 specifically from VIP interneurons replicates key neural and behavioral phenotypes observed following global Mecp2 loss of function.


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