Disruption of Foxg1 impairs neural plasticity leading to social and cognitive behavioral defects

• DOI: 10.1186/s13041-019-0484-x
• Publication Date: 2019-06-28T15:02:57Z
• Authors: Baocong Yu; Junhua Liu; Mingzhao Su; Chunlian Wang; Huanxin Chen; Chunjie Zhao
• Keywords: Dendritic Spines; Long-Term Potentiation; Nerve Tissue Proteins; Foxg1; Hippocampus; Receptors, N-Methyl-D-Aspartate; 03 medical and health sciences; Cognition; Dendritic arborization; Memory; Animals; Spatial learning and memory; Neural plasticity; RC346-429; Social Behavior; Mice, Knockout; 0303 health sciences; Neuronal Plasticity; Behavior, Animal; Research; FOXG1 syndrome; Forkhead Transcription Factors; Spine; Axons; Mice, Inbred C57BL; Neurology. Diseases of the nervous system

The transcription factor Foxg1 is known to be continuously expressed at a high level in mature neurons the telencephalon, but little about its role neural plasticity. Mutations human FOXG1 cause deficiencies learning and memory limit social ability, which defined as syndrome, pathogenic mechanism remains unclear. To examine of adults, we crossed Camk2a-CreER with Foxg1fl/fl mice conditionally disrupted tamoxifen neurons. We found that spatial were significantly impaired when examined by Morris water maze test. cKO also showed significant reduction freezing time during contextual cued fear conditioning test, indicating was affected. A remarkable Schaffer-collateral long-term potentiation recorded. Morphologically, dendritic arborization spine densities hippocampal pyramidal reduced. Primary cell culture further confirmed altered complexity after deletion. Our results indicated plays an important maintaining plasticity, vital high-grade function.