RT Journal Article
SR Electronic
T1 Hyperexcitability and Loss of Feedforward Inhibition Contribute to Aberrant Plasticity in the <em>Fmr1</em>KO Amygdala
JF eneuro
JO eNeuro
FD Society for Neuroscience
SP ENEURO.0113-21.2021
DO 10.1523/ENEURO.0113-21.2021
VO 8
IS 3
A1 Matthew N. Svalina
A1 E. Mae Guthman
A1 Christian A. Cea-Del Rio
A1 J. Keenan Kushner
A1 Serapio M. Baca
A1 Diego Restrepo
A1 Molly M. Huntsman
YR 2021
UL http://www.eneuro.org/content/8/3/ENEURO.0113-21.2021.abstract
AB Fragile X syndrome (FXS) is a neurodevelopmental disorder (NDD) characterized by intellectual disability, autism spectrum disorders (ASDs), and anxiety disorders. The disruption in the function of the FMR1 gene results in a range of alterations in cellular and synaptic function. Previous studies have identified dynamic alterations in inhibitory neurotransmission in early postnatal development in the amygdala of the mouse model of FXS. However, little is known about how these changes alter microcircuit development and plasticity in the lateral amygdala (LA). Using whole-cell patch clamp electrophysiology, we demonstrate that principal neurons (PNs) in the LA exhibit hyperexcitability with a concomitant increase in the synaptic strength of excitatory synapses in the BLA. Further, reduced feed-forward inhibition appears to enhance synaptic plasticity in the FXS amygdala. These results demonstrate that plasticity is enhanced in the amygdala of the juvenile Fmr1 knock-out (KO) mouse and that E/I imbalance may underpin anxiety disorders commonly seen in FXS and ASDs.