Not exact matches
The
protein's role in the pathway leading to memory impairment, however, remained unclear until scientists from IMCB utilised live - cell imaging techniques to elucidate the mechanism of memory impairment and illustrated
how SNX27 attributes to
synaptic dysfunction.
The team used genetics like a scalpel blade to remove individual
proteins from the synapse to identify their different roles within the synapse, and
how they maintain
synaptic transmission.
Learning more about
how synapses change their connections could help scientists better understand neurodevelopmental disorders such as autism, since many of the genetic alterations linked to autism are found in genes that code for
synaptic proteins.
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.
It is therefore essential to understand
how changes in
synaptic transmission can regulate the organization and dynamics of actin binding
proteins (ABPs).