The objective of this application is to elucidate the neural mechanisms important for recovery of acomplex learned behavior in the event of central damage. Zebra finches, like humans, have specific brainregions that are responsible for vocalization. I have found that microlesions in the anterior portion ofHVC(the zebra finch analogue of human cortical regions for speech production) induce a destabilization of thesong pattern. Over the course of two weeks, birds then recover most acoustic features of their song.Moreover, it appears that prior removal of LMAN (a telencephalic region necessary for adult vocalmaintenance) prevents HVC induced destabilization. This suggests a surprising interaction of telencephalicnuclei in the mediation and perhaps real-time sustainability of the adult song pattern. Thus, the proposedexperiments will examine integrated components and molecular changes involved in vocal recovery. Resultswill determine whether behavioral changes are enacted by neural repair mechanisms intrinsic to HVC, arapid change in the input from nuclei controlling song production, or a combination of both processes.Myfindings may have implications for recovery of vocal function following brain injury in humans.
Thompson, John A; Basista, Mark J; Wu, Wei et al. (2011) Dual pre-motor contribution to songbird syllable variation. J Neurosci 31:322-30 |
Wu, Wei; Thompson, John A; Bertram, Richard et al. (2008) A statistical method for quantifying songbird phonology and syntax. J Neurosci Methods 174:147-54 |
Thompson, John A; Wu, Wei; Bertram, Richard et al. (2007) Auditory-dependent vocal recovery in adult male zebra finches is facilitated by lesion of a forebrain pathway that includes the basal ganglia. J Neurosci 27:12308-20 |
Thompson, John A; Johnson, Frank (2007) HVC microlesions do not destabilize the vocal patterns of adult male zebra finches with prior ablation of LMAN. Dev Neurobiol 67:205-18 |