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SYNGAP1 Controls the Maturation of Dendrites, Synaptic Function, and Network Activity in Developing Human Neurons.
Nerea Llamosas1, Vineet Arora1, Ridhima Vij2,3
1Department of Neuroscience, Scripps Research, Jupiter, Florida 33458.
Summary
Loss of SYNGAP1 function in human neurons accelerates development, leading to larger cells, stronger synapses, and earlier network activity. This may explain SYNGAP1-related neurodevelopmental disorders.
Area of Science:
- Neuroscience
- Genetics
- Developmental Biology
Background:
- SYNGAP1 gene variants are linked to neurodevelopmental disorders like autism and epilepsy.
- Previous studies in rodent neurons showed SYNGAP1 regulates excitatory synapse development.
- The impact of SYNGAP1 loss-of-function on human neurons was previously unknown.
Purpose of the Study:
- To investigate the role of SYNGAP1 in the development and function of human neurons.
- To understand how SYNGAP1 loss-of-function affects neuronal structure and synaptic activity in human cells.
Main Methods:
- CRISPR/Cas9 technology was used to disrupt SYNGAP1 protein expression in human induced pluripotent stem cell (hiPSC)-derived neurons.
- Compared SYNGAP1-ablated neurons with isogenic control neurons.
- Analyzed dendritic morphogenesis, synapse formation, synaptic strength, and network activity.
Main Results:
- Neurons lacking SYNGAP1 showed enhanced dendritic growth and larger cell bodies.
- Increased numbers of excitatory synapses and earlier expression of synaptic activity were observed.
- SYNGAP1-null neurons exhibited earlier, elevated network spiking activity with increased bursting.
Conclusions:
- SYNGAP1 regulates the postmitotic maturation of human neurons derived from hiPSCs.
- Disruption of SYNGAP1 impacts neuronal development and the emergence of neural network activity.
- Altered neurodevelopmental processes due to SYNGAP1 dysfunction may contribute to associated disorders.
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