The design and assembly of neural circuits for vocal communication in songbirds

Unlike the human brain, which produces few neurons in adulthood, the brains of songbirds continue to produce new neurons throughout life. The function of these new neurons is not know, although it has been suggested that they endow the avian brain with a remarkable regenerative capacity that does not exist in mammals. It has also been proposed that the addition of new neurons in adulthood underlies behavioral plasticity, such as song learning. A better understanding of the cellular mechanisms that control the addition of new neurons to the postnatal brain may help clarify its biological function. This thesis is an investigation of the cell biology of postnatal neurogenesis in the songbird forebrain, with special emphasis on the High Vocal Center. Neuronal progenitors in the juvenile zebra finch brain were identified by fate mapping using engineered retroviruses. Multiple populations of neural progenitors appear to exist in the juvenile zebra finch brain, and each produces different types of neurons. At least three cell types appear to be added to the postnatal finch brain. Homology between neurogenesis in the postnatal finch and embryonic mammalian forebrain was also assessed. To characterize the mechanism of cell addition, videos were made, documenting the migration and integration of new neurons into the High Vocal Center. Neural progenitors were labeled using retroviruses, carrying the gene for the green fluorescent protein, allowing new neurons to be observed in the intact brain, with a powerful infrared laser. By replacing a small hole in the skull with a piece of optical glass, one could observe labeled neurons periodically over many days as they were born until they wired up to the existing circuitry. New neurons engaged in a previously undescribed form of migration. Further study of this form of neuron migration as well as other aspects of postnatal neurogenesis may lead to the development of strategies for replacing neurons in the human brain lost to death or disease.

Department dc:contributor.department

Massachusetts Institute of Technology. Dept. of Brain and Cognitive Sciences.

Grantor dc:publisher

Massachusetts Institute of Technology

Year dc:date.issued

2009

Author dc:creator

• Scott, Benjamin Barnett

Advisor dc:contributor.advisor

• Carlos Lois.

• Brain and Cognitive Sciences.

Statement dc:rights

• M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.

Licence dc:rights.uri

• http://dspace.mit.edu/handle/1721.1/7582

Language dc:language.iso

eng

Handle dc:identifier.uri

http://hdl.handle.net/1721.1/62984

OAI identifier oai:identifier

oai:dspace.mit.edu:1721.1/62984