Basolateral Amygdala Hyperexcitability is Associated With Precocious Developmental Emergence of Fear-Learning in Fragile X Syndrome

2021 ◽  
Author(s):  
Matthew N. Svalina ◽  
Christian Cea-Del Rio ◽  
Abigail Levy ◽  
Serapio M. Baca ◽  
E. Mae Guthman ◽  
...  
Keyword(s):  
Fragile X Syndrome ◽  
Basolateral Amygdala ◽  
Fragile X ◽  
Fear Learning

Pharmacological Rescue of Hippocampal Fear Learning Deficits in Fragile X Syndrome

2017 ◽  
Vol 55 (7) ◽  
pp. 5951-5961 ◽  
Author(s):  
Luis A. Martinez ◽  
Maria Victoria Tejada-Simon
Keyword(s):  
Fragile X Syndrome ◽  
Fragile X ◽  
Fear Learning ◽  
Learning Deficits

scholarly journals Deficient tonic GABAergic conductance and synaptic balance in the fragile X syndrome amygdala

2014 ◽  
Vol 112 (4) ◽  
pp. 890-902 ◽  
Author(s):  
Brandon S. Martin ◽  
Joshua G. Corbin ◽  
Molly M. Huntsman
Keyword(s):  
Intellectual Disability ◽  
Patch Clamp ◽  
Mouse Model ◽  
Fragile X Syndrome ◽  
Basolateral Amygdala ◽  
Fragile X ◽  
Brain Regions ◽  
Wild Type ◽  
Gabaergic Transmission ◽  
Whole Cell Patch Clamp

Fragile X syndrome (FXS) is the leading cause of inherited intellectual disability. Comorbidities of FXS such as autism are increasingly linked to imbalances in excitation and inhibition (E/I) as well as dysfunction in GABAergic transmission in a number of brain regions including the amygdala. However, the link between E/I imbalance and GABAergic transmission deficits in the FXS amygdala is poorly understood. Here we reveal that normal tonic GABAA receptor-mediated neurotransmission in principal neurons (PNs) of the basolateral amygdala (BLA) is comprised of both δ- and α5-subunit-containing GABAA receptors. Furthermore, tonic GABAergic capacity is reduced in these neurons in the Fmr1 knockout (KO) mouse model of FXS (1.5-fold total, 3-fold δ-subunit, and 2-fold α5-subunit mediated) as indicated by application of gabazine (50 μM), 4,5,6,7-tetrahydroisoxazolo[5,4- c]pyridin-3-ol (THIP, 1 μM), and α5ia (1.5 μM) in whole cell patch-clamp recordings. Moreover, α5-containing tonic GABAA receptors appear to preferentially modulate nonsomatic compartments of BLA PNs. Examination of evoked feedforward synaptic transmission in these cells surprisingly revealed no differences in overall synaptic conductance or E/I balance between wild-type (WT) and Fmr1 KO mice. Instead, we observed altered feedforward kinetics in Fmr1 KO PNs that supports a subtle yet significant decrease in E/I balance at the peak of excitatory conductance. Blockade of α5-subunit-containing GABAA receptors replicated this condition in WT PNs. Therefore, our data suggest that tonic GABAA receptor-mediated neurotransmission can modulate synaptic E/I balance and timing established by feedforward inhibition and thus may represent a therapeutic target to enhance amygdala function in FXS.

Fragile X syndrome, mental retardation and macroorchidism

1998 ◽  
Vol 54 (4) ◽  
pp. 366-367
Keyword(s):  
Mental Retardation ◽  
Fragile X Syndrome ◽  
Fragile X

Living with Fragile X Syndrome

2017 ◽  
Author(s):  
◽  
Rebecca Schira ◽  
Samantha Alexander ◽  
Noelani Brisbane ◽  
Kaitlyn Williams
Keyword(s):  
Fragile X Syndrome ◽  
Fragile X

Effects of Sertraline Treatment for Young Children with Fragile X Syndrome: Family Perspectives via Case Studies

2019 ◽  
Author(s):  
◽  
Tracy Ye ◽  
Decerie Mendoza ◽  
Elena Javier ◽  
Martina Dualan
Keyword(s):  
Young Children ◽  
Case Studies ◽  
Fragile X Syndrome ◽  
Fragile X ◽  
Family Perspectives

Fragile X Syndrome and Family Occupations

2019 ◽  
Author(s):  
Decerie Mendoza ◽  
Tracy Ye ◽  
Martina Dualan ◽  
Elena Javier
Keyword(s):  
Fragile X Syndrome ◽  
Fragile X
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