Andreas Frick, PhD Neurocentre Magendie Group ‘Circuit and dendritic mechanisms underlying cortical plasticity’ Inserm Unit 862, University of Bordeaux Tel: +33 (0)5 57 57 37 04 email@example.com
Recent estimates from the US Center for Disease Control suggest that one child in 68 suffers from Autistic Spectrum Disorders (ASD). ASD are neurological disorders characterised by a spectrum of symptoms, including problems with social interaction and communication, abnormal processing of sensory information, and stereotypic repetitive behaviours.
It has long been suggested that the brain of individuals with autism shows different connections. However, there is still no consensus either in regard to a model for these differences, or a possible link between these differences and the symptoms expressed by people suffering from these disorders.
A theory is currently emerging among neuroscientists at international level that suggests that the brain of individuals with ASD is “hyper-connected” at local level, but that overall, the different areas of the cortex are functionally “disconnected” from one another. The local connections can “process” a specific type of information (some aspects of vision, for instance). Conversely, longer range connections allow the brain to integrate more complex information from parts of the brain that often deal with different aspects. This latter type of connection is therefore needed for fine perception and understanding of our external environment.
Reorganisation of local and long-range connections in a mouse model of autism (right) and a wild-type mouse (left)
Neurons that become fluorescently labelled (in green) following injection of a tracker dye into the primary visual cortex (white arrow) send projections to the visual cortex and are distributed throughout different regions of the brain. In the fragile X mouse model (Fmr1-/y), one can observe a high density of neurons in the visual cortex (local connections), but a reduced number of neurons at a distance from this region (long-range connections).
Figure taken from Haberl et al. Science Advances 20 November 2015; 10.1126/sciadv.1500775. This figure is licensed under CC BY-NC. Modification of Figure 2a from the publication (modified thresholding and viewing angle, and removal of red mark indicating the point of injection).
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“Structural-functional connectivity deficits of neocortical circuits in the Fmr1−/y mouse model of autism” Matthias G. Haberl,1,2,3* Valerio Zerbi,4† Andor Veltien,4 Melanie Ginger,1,2 Arend Heerschap,4 Andreas Frick1,2‡ 1Inserm, Neurocentre Magendie, Physiopathologie de la plasticité neuronale, U862, Bordeaux, France. 2University of Bordeaux, Neurocentre Magendie, Physiopathologie de la plasticité neuronale, U862, Bordeaux, France. 3Institute of NeuroInformatics, University of Zurich, Zurich, Switzerland. 4Biomedical Magnetic Resonance, Department of Radiology and Nuclear Medicine, Radboud University Medical Center, Nijmegen,Netherlands. *Present address: National Center for Microscopy and Imaging Research, Center for Research in Biological Systems, University of California San Diego, School of Medicine, La Jolla, CA, USA. †Present address: Neural Control of Movement Lab, Department of Health Sciences and Technology, ETH Zürich, Winterthurerstrasse 190, 8057 Zurich, Switzerland. Science Advances 20 November 2015