Neuron Signaling Persists, Faintly, Even When Key Presynaptic Proteins Are Absent

Results from experiments in mice revise a long-held hypothesis that certain protein scaffolds are needed for synaptic activity.

Ben Andrew Henry
Oct 31, 2016

DOCKED: Vesicles continue to release neurotransmitters into the synapse even after researchers disable docking scaffolds.© ISTOCK.COM/COSMIN4000

EDITOR'S CHOICE IN NEUROSCIENCE

The paper
S.S.H. Wang et al., “Fusion competent synaptic vesicles persist upon active zone disruption and loss of vesicle docking,” Neuron, 91:777-91, 2016.

Hair trigger
Neurons send each other signals by firing neurotransmitters across synapses. A stash of neurotransmitter-packed vesicles hunkers close to the presynaptic membrane so the vesicles can fuse with the membrane and release their cargo as soon as an electrical impulse pulls the trigger. An elaborate scaffold of proteins coordinates this vesicle docking, and scientists long assumed these proteins were essential to neuron signaling. For years, Harvard Medical School neuroscientist Pascal Kaeser has wanted “to test that very fundamental hypothesis” by “entirely [removing] that structure.”

Still talking
Kaeser and his colleagues recently got their chance. By genetically altering mice to disable key scaffolding proteins, they...