Philipp Schnepel, Max Delbrück Center for Molecular Medicine, Berlin | Hyperexcitability in Mouse Models of Autism-Spectrum Disorders
| When |
May 23, 2017
from 05:15 PM to 06:45 PM |
|---|---|
| Where | BCF Lecture Hall, Hansastr. 9a |
| Contact Name | Prof. Dr. Ad Aertsen |
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Abstract
Autism Spectrum Disorder (ASD) is a genetically heterogeneous disorder for which the causal mechanism remains unidentified. It is hypothesized that a common pathology exists that is defined by an increased excitation-inhibition (E-I) ratio and hyperexcitability at the neural circuit level. Reports on deficits in interneuron number and of increased E-I ratio collectively suggest circuit excitability in ASD1-7 . To test this model, we are comparing local circuit physiology and sensory processing in primary somatosensory (S1) cortex across multiple ASD model mouse strains. S1 is a reasonable site to investigate ASD circuit dysfunction since 80-90% of ASD patients show sensory abnormalities including tactile hypersensitivity 8 . Here, we report initial results from three ASD strains: contactin associated protein-like 2 (Cntnap2), fragile X mental retardation 1 (Fmr1) and microdeletion on chromosome 16 (16p11.2) mice. Although whole-cell recordings in L2/3 of S1 slices indicate an increase in E-I-ratio, in vivo extracellular recordings show heterogeneous results across the different strains, suggesting that the hyperexcitability hypothesis needs to be revisited as a general mechanism for autism-spectrum disorders.
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