AI Article Synopsis
- * Researchers discovered that many autism and schizophrenia risk genes are active in a specific brain area (anterodorsal thalamic nuclei) linked to learning and memory, and manipulating these genes caused memory deficits.
- * The study identifies distinct roles for the anterodorsal and anteroventral thalamic subdivisions in memory processes and shows that addressing neuronal hyperexcitability linked to certain risk genes can improve memory deficits.
Article Abstract
Neuropsychiatric disorders are often accompanied by cognitive impairments/intellectual disability (ID). It is not clear whether there are converging mechanisms underlying these debilitating impairments. We found that many autism and schizophrenia risk genes are expressed in the anterodorsal subdivision (AD) of anterior thalamic nuclei, which has reciprocal connectivity with learning and memory structures. CRISPR-Cas9 knockdown of multiple risk genes selectively in AD thalamus led to memory deficits. While the AD is necessary for contextual memory encoding, the neighboring anteroventral subdivision (AV) regulates memory specificity. These distinct functions of AD and AV are mediated through their projections to retrosplenial cortex, using differential mechanisms. Furthermore, knockdown of autism and schizophrenia risk genes PTCHD1, YWHAG, or HERC1 from AD led to neuronal hyperexcitability, and normalization of hyperexcitability rescued memory deficits in these models. This study identifies converging cellular to circuit mechanisms underlying cognitive deficits in a subset of neuropsychiatric disease models.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8376805 | PMC |
| http://dx.doi.org/10.1016/j.neuron.2021.06.005 | DOI Listing |
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