| Autor: |
Svalina, Matthew N., Cea-Del Rio, Christian A., Kushner, J. Keenan, Levy, Abigail, Baca, Serapio M., Guthman, E. Mae, Opendak, Maya, Sullivan, Regina M., Restrepo, Diego, Huntsman, Molly M. |
| Předmět: |
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| Zdroj: |
Journal of Neuroscience; 9/21/2022, Vol. 42 Issue 38, p7294-7308, 15p |
| Abstrakt: |
Fragile X Syndrome is a neurodevelopmental disorder and the most common monogenic cause of intellectual disability, autism spectrum disorders, and anxiety disorders. Loss of fragile x mental retardation protein results in disruptions of synaptic development during a critical period of circuit formation in the BLA. However, it is unknown how these alterations impact microcircuit development and function. Using a combination of electrophysiologic and behavioral approaches in both male (Fmr1-/y) and female (Fmr1−/−) mice, we demonstrate that principal neurons in the Fmr1KO BLA exhibit hyperexcitability during a sensitive period in amygdala development. This hyperexcitability contributes to increased excitatory gain in fear-learning circuits. Further, synaptic plasticity is enhanced in the BLA of Fmr1KO mice. Behavioral correlation demonstrates that fear-learning emerges precociously in the Fmr1KO mouse. Early life 4,5,6,7-tetrahydroisoxazolo [5,4-c]pyridin-3ol intervention ameliorates fear-learning in Fmr1KO mice. These results suggest that critical period plasticity in the amygdala of the Fmr1KO mouse may be shifted to earlier developmental time points. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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