Zebra finch songs and brain research
Chirp-happy canaries grow silent in the fall when cells in the brain's vocal center die off. When December rolls around, though, cell rebirth resumes, and in springtime the chorus is back in session. Zebra finches, on the other hand, are small songbirds that are close cousins of canaries, and can string together a highly complicated song, but do not have the seasonal replacement of this song circuitry. This limitation of brain cell reproduction is more similar to that of mammals, including humans.
This observation prompted Jeffrey Macklis, MD, and his colleagues to investigate in zebra finches whether cell death can lead to the recruitment of new nerve cells, or neurons, that take up the very same activity. While the songbird brain is not directly comparable to the mammalian brain, it shares many common features, and Macklis and his team suspected analogies between the two species' abilities. Their findings may contribute over the coming decades to potential treatments for patients with cerebral palsy, spinal cord injuries, amyotrophic lateral sclerosis (ALS), Huntington's disease and Alzheimer's disease.
To test their hypothesis, the researchers induced the death of song neurons in the zebra finches' brain using some very special biophysical and molecular approaches. Indeed, the number of new brain neurons that were recruited from resident precursors, or stem cells, directly correlated with the number that were killed. These new neurons sent long connections to the correct location in the fully formed brain, and after four months, the zebra finches were singing again.
The team also more recently showed the even more remarkable result that, in the adult mouse, induced neuron death can lead to development of replacement neurons when the right multipotent precursor cells, which are responsible for initial development of neurons in the brain, are present. They induced precursor cells in the cerebral cortex of adult mice to replace damaged neurons, and now have turned their attention to understanding the molecular mechanisms and genes involved’Äîlikely a very complex set’Äî during this process.
"The types of neurons we are studying in the mouse are involved in a variety of developmental and neurodegenerative diseases of the nervous system in humans. Some of the cells we investigated in zebra finches bear a direct relation to those that degenerate in Huntington's and other nervous system diseases. In all of these systems, it has previously been believed that nerve damage could not be reversed," says Macklis. "None of these will be ready for human application for several years’Äîthis work will likely come to fruition over the coming decades. But, instead of being absolutely unthinkable, in my cautious, optimistic belief, it will come to be."
