Fragile X Syndrome Research Today is a free monthly online journal that collates and summarizes the latest research about Fragile X Syndrome, including details on symptoms, treatment, heritability, diagnosis.

Major defects in neocortical GABAergic inhibitory circuits in mice lacking the fragile X mental retardation protein.

Selby L, Zhang C, Sun QQ

Department of Zoology and Physiology, University of Wyoming, Laramie, WY 82071, United States.

This study focused on the cytoarchitectonic and morphological differences in GABA-releasing interneurons between adult Fmr1 knock-out (FMR1KO) and wild-type (WT) mice in the somatosensory cortex. Our results showed a robust reorganization of neocortical, but not hippocampal inhibitory circuits in the FMR1KO mouse. The reorganization is characterized by a significant reduction (20%, p<0.001) in the densities of parvalbumin (PV)-positive, but not calbindin (CB) and calretinin (CR)-positive interneurons. A significant enlargement of soma size and an altered lamina distribution of PV but not CR and CB cells was also observed. Additionally, there was a modest but significant increase in TrkB-immunoreactivity in PV-positive cells in the FMR1KO mouse. These results provide the first report showing significant alterations of GABA-releasing interneurons in the mouse model of fragile X syndrome. Uncovering the changes in specific GABAergic inhibitory circuits could help understand mechanisms underlying the behavior deficits of fragile X syndrome and autism.

Published 23 January 2007 in Neurosci Lett, 412(3): 227-32.
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