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Regulation of excitatory presynaptic activity by Ambra1 protein determines neuronal networks in sex-dimorphic manner

MPS-Authors
/persons/resource/persons182225

Ju,  Anes
Research Group of Clinical Neuroscience, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

/persons/resource/persons182066

Altas,  Bekir
Department of Molecular Neurobiology, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

/persons/resource/persons203529

Rhee,  Hong Jun
Department of Molecular Neurobiology, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

/persons/resource/persons182403

Schwark,  Manuela
Department of Molecular Neurobiology, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

/persons/resource/persons182183

Hassouna,  Imam
Research Group of Clinical Neuroscience, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

/persons/resource/persons203090

Sigler,  Albrecht
Department of Molecular Neurobiology, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

/persons/resource/persons182236

Kawabe,  Hiroshi
Department of Molecular Neurobiology, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

/persons/resource/persons14945

Chowdhury,  K.
Department of Molecular Neurobiology, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

/persons/resource/persons182138

Ehrenreich,  Hannelore
Research Group of Clinical Neuroscience, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

/persons/resource/persons182104

Brose,  Nils
Department of Molecular Neurobiology, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

/persons/resource/persons182371

Rhee,  Jeong Seop
Department of Molecular Neurobiology, Max Planck Institute for Multidisciplinary Sciences, Max Planck Society;

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Citation

Ju, A., Altas, B., Rhee, H. J., Schwark, M., Hassouna, I., Sigler, A., et al. (2023). Regulation of excitatory presynaptic activity by Ambra1 protein determines neuronal networks in sex-dimorphic manner. bioRxiv. doi:10.1101/2022.12.19.521004.


Cite as: https://hdl.handle.net/21.11116/0000-000D-7B50-F
Abstract
Heterozygous mutation of Ambra1, known as a positive autophagy regulator, produces autismlike behavior in mice and autistic phenotypes in humans in a female-specific manner. However, the substantial roles of the Ambra1 mutation in neurons are still unknown. We find that Ambra1 heterozygotes display a moderate decrease in excitatory synaptic release in-vitro and ex-vivo exclusively in females without autophagy activity, resulting in significant alterations in γ-oscillation power and seizure susceptibility by excitatory/inhibitory (E/I) imbalance. Specifically, Ambra1 deficiency has no effect on neurogenesis and morphogenesis, but selectively decreases excitatory synaptic activity without changes in synapse number, quantal size, synaptic release probability, and synaptic plasticity. Therefore, the limited excitatory synaptopathy by Ambra1 expression levels ultimately determines E/I imbalance in global neural networks leading to the female-specific ASD.