AI Article Synopsis
- The study explores how fragile X syndrome, caused by the lack of FMRP, affects structural plasticity and learning in the adult brain, particularly focusing on olfactory bulb neurons.
- Using an olfactory learning task and specific mouse models, researchers found that learning triggers significant changes in neuron structure that are impaired without FMRP, but can be restored with certain treatments.
- The findings suggest that FMRP plays a crucial role in mediating structural changes during olfactory learning by regulating local translation of αCaMKII, which may have implications for understanding autism spectrum disorders, especially fragile X syndrome.
Article Abstract
Background: In the adult brain, structural plasticity allowing gain or loss of synapses remodels circuits to support learning. In fragile X syndrome, the absence of fragile X mental retardation protein (FMRP) leads to defects in plasticity and learning deficits. FMRP is a master regulator of local translation but its implication in learning-induced structural plasticity is unknown.
Methods: Using an olfactory learning task requiring adult-born olfactory bulb neurons and cell-specific ablation of FMRP, we investigated whether learning shapes adult-born neuron morphology during their synaptic integration and its dependence on FMRP. We used alpha subunit of the calcium/calmodulin-dependent kinase II (αCaMKII) mutant mice with altered dendritic localization of αCaMKII messenger RNA, as well as a reporter of αCaMKII local translation to investigate the role of this FMRP messenger RNA target in learning-dependent structural plasticity.
Results: Learning induces profound changes in dendritic architecture and spine morphology of adult-born neurons that are prevented by ablation of FMRP in adult-born neurons and rescued by an metabotropic glutamate receptor 5 antagonist. Moreover, dendritically translated αCaMKII is necessary for learning and associated structural modifications and learning triggers an FMRP-dependent increase of αCaMKII dendritic translation in adult-born neurons.
Conclusions: Our results strongly suggest that FMRP mediates structural plasticity of olfactory bulb adult-born neurons to support olfactory learning through αCaMKII local translation. This reveals a new role for FMRP-regulated dendritic local translation in learning-induced structural plasticity. This might be of clinical relevance for the understanding of critical periods disruption in autism spectrum disorder patients, among which fragile X syndrome is the primary monogenic cause.
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| http://dx.doi.org/10.1016/j.biopsych.2015.07.023 | DOI Listing |
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