Neural circuit architecture defects in a Drosophila model of Fragile X syndrome are alleviated by minocycline treatment and genetic removal of matrix metalloproteinase.

Moreover, the accumulation of developmentally arrested satellite boutons at the dfmr1 50M null synapse was fully restored to control levels (control: 1.9±0.25, dfmr1 : 4.1±0.39, P ≤0.001; dfmr1 + minocycline: 1.83±0.30, n =12), a highly significant effect ( P ≤0.001; Fig. 1B,D ).

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