Max Planck Institute for Dynamics and Self-Organization -- Department for Nonlinear Dynamics and Network Dynamics Group
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Tuesday, 30.04.2013 17 c.t.

A specific deficit in auditory adaptation in a mouse model of human neurodevelopmental disorders

by Dr. Jennifer Linden
from The Ear Institute, Faculty of Brain Sciences, UCL Ear Institute, London, UK

Contact person: Dominika Lyzwa


MPI DS seminar room (0.77/0.79)


Neurodevelopmental disorders such as specific language impairment and dyslexia have been proposed to be associated with various physiological and anatomical risk factors, including auditory temporal processing deficits, autoimmune disorders, and the development of neocortical "ectopias" (displaced nests of neurons in the cortex). These associations remain highly controversial, in part because the complex human symptoms of neurodevelopmental disorders are difficult or impossible to assess in animal models of the proposed risk factors. However, it is possible to examine neural abnormalities in animal models of the risk factors, such as the BXSB/MpJ-Yaa mouse model of auditory temporal processing deficits, autoimmune disorders, and neocortical ectopias. BXSB/MpJ-Yaa mice (male mice of the inbred BXSB/MpJ strain) develop autoimmune disease early in adulthood, and nearly half the animals also have neocortical ectopias, indicating abnormal thalamocortical development. Although the ectopias are in motor cortex, not in auditory cortex, ectopic BXSB/MpJ-Yaa mice are reported to have more difficulty perceiving rapid changes in sound than their non-ectopic BXSB/MpJ-Yaa littermates. The exact nature and origin of this auditory processing deficit is unknown. In this talk, I will show that ectopic male BXSB/MpJ mice have an extremely specific neural processing abnormality. In vivo extracellular recordings from auditory thalamic neurons revealed that neural thresholds for detection of a very brief gap in noise were significantly higher in ectopic than non-ectopic BXSB/MpJ-Yaa animals in two out of the three main subdivisions of the auditory thalamus. However, auditory thalamic responses to equally rapid click sequences were not significantly different between ectopic and non-ectopic BXSB/MpJ-Yaa mice in any of the thalamic subdivisions. Moreover, thalamic responses to click and tone stimuli, and electroencephalographic measures of peripheral and brainstem auditory sensitivity, were indistinguishable between ectopic and non-ectopic animals. These results indicate that ectopic BXSB/MpJ-Yaa mice do not have a general auditory temporal processing deficit, but a specific deficit in auditory adaptation to noise --- and that this deficit affects only a subset of central auditory structures. The findings therefore suggest that neurodevelopmental disorders may be associated with subtle abnormalities in central auditory processing that would not be detected by standard clinical measures of hearing sensitivity.

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