Enriched environment promotes behavioral and morphological recovery in a mouse model for the fragile X syndrome.

Autor: Restivo, Leonardo, Ferrari, Francesca, Passino, Enrica, Sgobio, Carmelo, Bock, Jörg, Oostra, Ben A., Bagni, Claudia, Ammassari-Teule, Martine
Předmět:
Zdroj: Proceedings of the National Academy of Sciences of the United States of America; 8/9/2005, Vol. 102 Issue 32, p11557-11562, 6p
Abstrakt: Fragile X syndrome, the most frequent form of hereditary mental retardation, is due to a mutation of the fragile X mental retardation 1 (FMR1) gene on the X chromosome. Like fragile X patients, FMR1-knockout (FMR1-KO) mice lack the normal fragile X mental retardation protein (FMRP) and show both cognitive alterations and an immature neuronal morphology. We reared FMR1-KO mice in a C57BL/6 background in enriched environmental conditions to examine the possibility that experience-dependent stimulation alleviates their behavioral and neuronal abnormalities. FMR1-KO mice kept in standard cages were hyperactive, displayed an altered pattern of open field exploration, and did not show habituation. Quantitative morphological analyses revealed a reduction in basal dendrite length and branching together with more immature-appearing spines along apical dendrites of layer five pyramidal neurons in the visual cortex. Enrichment largely rescued these behavioral and neuronal abnormalities while increasing α-amino- 3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor subunit 1 (GluR1) levels in both genotypes. Enrichment did not, however, affect FMRP levels in the WT mice. These data suggest that FMRP-independent pathways activating glutamatergic signaling are preserved in FMR1-KO mice and that they can be elicited by environmental stimulation. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index