Presynaptic Rac1 controls synaptic strength through the regulation of synaptic vesicle priming

What is it about?

Neuronal communication relies on specialized structures on nerve cells called synapses which contain synaptic vesicles filled with neurotransmitters. These synaptic vesicles are released upon neuronal activity. For the brain to communicate effectively, synaptic vesicles need to be released and refilled in a highly coordinated manner. A molecule called Rac1 controls how things move around in the synapses. It is important for building connections in the brain but we don't know much about how Rac1 affects the release and refilling of these vesicles. To study the role of Rac1 in synaptic transmission, we removed the protein from only the presynaptic terminal of a particular cell type, leaving the rest of the brain unaffected. Using an experimental approach to measure the number of synaptic vesicles released in combination with computational models, we found that the removal of Rac1 increases the strength of the synapse, but leads to a loss of temporal precision, potentially lowering the brains ability to react to sensory information.

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