Mechanical actions of dendritic-spine enlargement on presynaptic exocytosis
Communication between neurons in the brain is generally associated with electrochemical signaling. Haruo Kasai’s laboratory discovered that dendritic spines could be stimulated to enlarge rapidly, which at the time they hypothesized could result in pressing against the presynaptic boutons in the synaptic junction and elicit an effect; however, at the time the tools to effectively investigate this phenomenon wasn’t available. In this recent study, the group validated their theory that physical forces elicited by dendritic spine enlargement can produce mechanosensory force signals in presynaptic boutons. In order to effectively investigate this phenomenon they utilized three novel technologies including a novel fluorescent protein called iFLuSnFR that detects glutamate release, an imaging technique to track SNARE complex assembly, and their tools to optogenetically induce action potentials in presynaptic neurons. They showed that force manipulation using fine and transient pushing of the presynaptic boutons with a glass pipette markedly promotes both the evoked release of glutamate and the assembly of SNARE proteins that is dependent on actin polymerization. This mechanism could also be induced by regulation of osmotic pressure changes. Importantly, they showed that spine enlargement induced by two-photon glutamate uncaging produced these forced induced effects only when the spines pushed the boutons by their elongation. The group showed for the first time that synaptic transmission occurred through mechanical forces. Cytoskeleton’s non-muscle beta-actin (Cat. # APHL99) was used in this study to help define the role actin plays in this mechanosensory mechanism.
Schematic of spine enlargement and its effect on the presynaptic bouton