"This allows us to directly visualize the addition of these receptors to the spine surface from their internal stores," he says.
The researchers tested how the movement of the receptors was tied to remodeling of the internal skeleton of the cell, by using drugs that either loosen or freeze the actin cytoskeleton, which forms the main structural support inside dendritic spines.
They then investigated the family of proteins called ADF (actin depolymerizing factor)/cofilin, which Zheng describes as acting like a pair of scissors, severing the links of the actin cytoskeleton.
"Our results suggest that there are two activities that need to be coordinated to strengthen dendritic spines: the cell has to cut actin filaments in order to allow receptors in storage to be added to the surface, but then it has to put away the scissors and stabilize and enlarge the spines," Zheng says.
Williams syndrome is a rare developmental disorder caused by a chromosomal deletion spanning 28 genes, several of which may contribute to changes in cognitive development. One of the genes thought to be responsible encodes the enzyme LIM kinase 1. LIM kinase deactivates ADF/cofilin, which means neurons in Williams syndrome may have an altered ability to remodel dendritic spines.
Williams syndrome impairs affected individuals' perceptions of space as well as their ability to make social judgments, but tends to leave other functions relatively intact. Individuals with Williams syndrome are noted to have an affinity for language and music.
"Cytoskeletal remodeling is required for some aspects of long-term potentiation but also needs to be reigned in. If we change LIM kinase or ADF/cofilin and shift the balance of the cytoskeletal remodeling, that could affect some cognitive processes and not others," Zheng proposes. He also believes that the
|Contact: Holly Korschun|