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  3. SCSB Lunch Series: Thalamic reticular nucleus dysfunction in neurodevelopmental disorders
Feng-headshot-2017-2.jpg
Simons Center for the Social Brain
Lunch Series

SCSB Lunch Series: Thalamic reticular nucleus dysfunction in neurodevelopmental disorders

Speaker(s)
Guoping Feng, Ph.D.
Add to CalendarAmerica/New_YorkSCSB Lunch Series: Thalamic reticular nucleus dysfunction in neurodevelopmental disorders12/14/2018 5:00 pm12/14/2018 6:00 pmSimons Center Conference room 46-6011
December 14, 2018
5:00 pm - 6:00 pm
Location
Simons Center Conference room 46-6011
Contact
Alexandra Sokhina
    Description

    Date: Friday, December 14, 2018
    Time: 12:00pm – 1:00pm
    Location: Simons Center Conference Room, Building 46, Room 6011, 6th Floor, MIT (43 Vassar Street, Cambridge, 02139 MA)

    Speaker: Guoping Feng, Ph.D.
    Affiliation: Poitras Chair Professor of Neuroscience, McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, MIT; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard.

    Talk title: Thalamic reticular nucleus dysfunction in neurodevelopmental disorders

    Abstract: The Thalamic reticular nucleus (TRN) provides major inhibitory inputs to the thalamus and plays important roles in sensory gating, attention selection and sleep rhythms. Many of the risk genes for ASD, schizophrenia and ADHD are highly expressed in the TRN, raising the possibility that TRN may be a circuit converging point for some of the overlapping behavioral abnormalities in these disorders. Using TRN-specific genetic deletions in mice, we demonstrate the critical roles of TRN dysfunction in attention deficit, hyperactivity and sleep disruption, commonly observed in neurodevelopmental disorders including ASD. Using multi-scale single cell analysis including single cell RNA-Seq, multiplex RNA FISH, electrophysiological recordings and molecular tracing. We identified two major TRN neuronal subtypes that have distinct electrophysiological properties, differential topographic connectivity related to different thalamic sensory modalities, i.e. first order and high order thalamic nuclei. Through such non-overlapping anatomical pathways mediated by its subpopulations, TRN might differentially tune incoming sensory information through thalamo-cortical circuits. Importantly, we identified genes selectively expressed by each of the TRN subtypes of neurons, paving the way for testing molecular targets that could potentially regulate different TRN functions based on their thalamic connectivity.

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