Rutgers' Bonnie Firestein likens nerve cells to trees -- some are short and bushy with many branches while others are tall with a few branches coming out of one or two main trunks. Different branching patterns correlate with specific disorders and Firestein's quest is to discover how these dissimilar patterns come about and why.
A new paper by Firestein and her colleagues at Rutgers, The State University of New Jersey, examines the role of the protein snapin in nerve branch, or dendrite, patterning and its potential as a drug target in therapies aimed at learning and memory disorders. The article will appear in the journal Molecular Biology of the Cell.
While disorders like autism may arise from a multiplicity of causes, research at the cellular level, such as that of Firestein and her Rutgers team, is creating an important point of entry for early intervention with therapeutic drugs.
Dendrites are the input centers of neurons -- where nerve cells receive information that they pass on to another nerve cell or to the brain. When there is an abnormal decrease in dendrite branches, there are fewer sites to receive information and communication may be impeded. Individuals with disorders such as autism and Rett syndrome display not only fewer branches, but also show two quite different dendrite patterns. Firestein's most recent work explores the how and why of dendrite branching and patterning.
"It's not just how many branches there are, but where they are and the pattern they form," said Firestein, an assistant professor in Rutgers' department of cell biology and neuroscience. "The patterning actually affects the way a cell signals and understanding the patterning could be just as important as understanding how many branches are there. Ultimately, this could lead to new drugs designed to modulate the patterning activity."
Firestein has worked extensively with cypin, a protein that regulates dendrite numbers, Cypin works on tubulin, a protein that is a structural building block of the dendrite skeleton. Now Firestein's research group has turned its attention to the protein snapin. When snapin binds to cypin, tubulin is crowded out, so fewer dendrites assemble and more branching occurs.