The songbird zebra finch is an exemplary model system in which to study trial-and-error learning, as the bird learns its single song gradually through the production of many noisy renditions. It is also a good system in which to study the maintenance of motor skills, as the adult bird actively maintains its song and retains some residual plasticity. Motor learning occurs through the association of timing within the song, represented by sparse firing in nucleus HVC, with motor output, driven by nucleus RA. Here we show through modeling that the small level of observed variability in HVC can result in a network which is more easily able to adapt to change, and is most robust to cell damage or death, than an unperturbed network. In collaboration with Carlos Lois’ lab, we also consider the effect of directly perturbing HVC through viral injection of toxins that affect the firing of projection neurons. Following these perturbations, the song is profoundly affected but is able to almost perfectly recover. We characterize the changes in song acoustics and syntax, and propose models for HVC architecture and plasticity that can account for some of the observed effects. Finally, we suggest a potential role for inputs from nucleus Uva in helping to control timing precision in HVC.

During conversations we rapidly switch between listening and speaking which often requires withholding or delaying our speech in order to hear others and avoid overlapping. This capacity for vocal turn-taking is exhibited by non-linguistic species as well, however the neural circuit mechanisms that enable us to regulate the precise timing of our vocalizations during interactions are unknown. We aim to identify the neural mechanisms underlying the coordination of vocal interactions. Therefore, we paired zebra finches with a vocal robot (1Hz call playback) and measured the bird’s call response times. We found that individual birds called with a stereotyped delay in respect to the robot call. Pharmacological inactivation of the premotor nucleus HVC revealed its necessity for the temporal coordination of calls. We further investigated the contributing neural activity within HVC by performing intracellular recordings from premotor neurons and inhibitory interneurons in calling zebra finches. We found that inhibition is preceding excitation before and during call onset. To test whether inhibition guides call timing we pharmacologically limited the impact of inhibition on premotor neurons. As a result zebra finches converged on a similar delay time i.e. birds called more rapidly after the vocal robot call suggesting that HVC inhibitory interneurons regulate the coordination of social contact calls. In addition, we aim to investigate the vocal turn-taking capabilities of the common nightingale. Male nightingales learn over 100 different song motifs which are being used in order to attract mates or defend territories. Previously, it has been shown that nightingales counter-sing with each other following a similar temporal structure to human vocal turn-taking. These animals are also able to spontaneously imitate a motif of another nightingale. The neural mechanisms underlying this behaviour are not yet understood. In my lab, we further probe the capabilities of these animals in order to access the dynamic range of their vocal turn taking flexibility.