Research on components of the brain's electrical signaling system has answered a basic question about our human evolution, confirming scientific belief that we two-legged, computer-using creatures are descended from prokaryotes -- cellular organisms so primitive and simple that they exist without nuclei or cell walls.
The study, led by Zhe Lu, MD, PhD, an Associate Professor in the Department of Physiology at the University of Pennsylvania School of Medicine were recently published in the journal Nature.The research by Lu and his colleagues focused on the structure and function of molecules called potassium channels, which are essential to how the brain works. When potassium channels open and close, they control the flow of potassium ions across cell membranes. The current contributes to the electrical signals in nerve, muscle and endocrine cells.
Scientists who study the brain's electrical signals have relied on a blue-print developed from functional studies of eukaryotic (neuronal) potassium channels and structural studies of prokaryotic (bacterial) potassium channels, based on the assumption that the two channels are essentially the same. However this assumption has recently been challenged.
Lu and his collaborators devised a project in which the pore of a prokaryote's potassium channel (the interior core of the channel) was substituted for the pore of a potassium channel in a euokaryote. The scientists found that the eukarotic channel continued to function essentially as it had previous to the substitution.
"This has very profound implications for evolution," Lu said. "It appears the potassium channels in advanced brains and hearts of mammals have evolved from something like this bacterial channel. So what we learn from the more easily studied bacterial channels can be directly applied to our understanding of potassium channels in human brains."
In the study, Lu worked with Penn colleagues Angela Klem, research specialist, and Yajamana Ramu, PhD. The work was funded by the National Institutes of Health. - By Ellen O'Brien
[Contact: Ellen O'Brien]
09-Nov-2001