During an action potential, calcium influx into the presynaptic terminal triggers the fusion of
synaptic vesicles with the plasma membrane, leading to the release of transmitter through the process of exocytosis.
Before the fusion of
synaptic vesicles with the plasma membrane, a protein complex is thought to form between VAMP — an integral membrane protein of the vesicle — and two proteins associated with the plasma membrane, SNAP - 25 and syntaxin.
Voltage-gated calcium channels can not form properly when cacophony is mutated, preventing fusion of
the synaptic vesicle with the plasma membrane and neurotransmitter release.
Not exact matches
Fluorescently labeled
synaptic vesicles inside the axons of cultured neurons were recorded
with stimulated emission depletion (STED) microscopy in a 2.5 - micrometer by 1.8 - micrometer field of view.
This allows
synaptic vesicles filled
with neurotransmitter to fuse
with the plasma membrane and release the neurotransmitters into the
synaptic cleft.
I ache to see your action potential in action To be blinded by the searing speed of your electric signal As it sparks from node to node To behold the violent beauty of
vesicles fusing
with your presynaptic membrane — Pouring their contents into your
synaptic cleft How I wish to be your postsynaptic cell So that I may be flooded by your molecules
The structure of synaptophysin suggests that the protein may function as a channel in the
synaptic vesicle membrane,
with the carboxyl terminus serving as a binding site for cellular factors.
Synaptic vesicles are chock - full
with neurotransmitters and release them by fusing
with the presynaptic plasma membrane.
During this time, we together
with our long - time collaborators Reinhard Jahn and Jose Rizo, and in parallel
with Richard Scheller and others, discovered the role of SNARE and SM proteins in
synaptic vesicle fusion.
Beginning in 1988 Scheller, then at Stanford, succeeded in characterizing several key proteins necessary for
synaptic vesicle fusion
with the presynaptic membrane, the prerequisite step for neurotransmitter release.
This was found to interfere
with the same mechanism, essentially by impairing the ability of alpha - synuclein to regulate the flow of
synaptic vesicles, and hence compromising the signalling between neurons.
The next major advance which moved this analysis from a cell physiological to a molecular level was accomplished by Scheller and Südhof who made overlapping contributions that characterized the proteins that controlled the two key steps of transmitter release: 1) They showed the mechanism by which the
vesicle is mobilized to the release sites of the presynaptic terminal, where the
synaptic vesicle first fuses
with the membrane of the sending neuron and then leaves the cell, and 2) they also discovered how Ca2 + drives the
vesicle to release its contents.
Channels, which allow a compound such as glutamate to move from a compartment
with high concentrations to one
with low concentrations, but not vice versa, can not pump as large amounts of a compound into
synaptic vesicles as a transporter can.
«Without this specialized neurotransmitter recycling and endocytosis,
synaptic vesicles are not recycled fast enough to keep up
with nerve and muscle cell activity,» she said.
Electron microscopic studies revealed that the presynaptic terminal of the neuron transmitting the information is filled
with synaptic vesicles, small organelles containing thousands of molecules of a chemical neurotransmitter.
Richard Scheller has used a combination of biochemistry, molecular biology, and cell biology to identify several key
synaptic vesicle and plasma membrane proteins involved in fusion of the neurotransmitter - containing
vesicles with the membrane of the presynaptic terminal.