Search for: All records

Understanding the sensorimotor control of the endless variety of human speech patterns stands as one of the apex problems in neuroscience. The capacity to learn – through imitation – to rapidly sequence vocal sounds in meaningful patterns is clearly one of the most derived of human behavioral traits. Selection pressure produced an analogous capacity in numerous species of vocal-learning birds, and due to an increasing appreciation for the cognitive and computational flexibility of avian cortex and basal ganglia, a general understanding of the forebrain network that supports the learning and production of birdsong is beginning to emerge. Here, we review recent advances in experimental studies of the zebra finch (Taeniopygia guttata), which offer new insights into the network dynamics that support this surprising analogue of human speech learning and production. 

Song learning in zebra finches (Taeniopygia guttata) requires exposure to the song of a tutor, resulting in an auditory memory. This memory is the foundation for later sensorimotor learning, resulting in the production of a copy of the tutor's song. The cortical premotor nucleus HVC (proper name) is necessary for auditory and sensorimotor learning as well as the eventual production of adult song. We recently discovered that the intrinsic physiology of HVC neurons changes across stages of song learning, but are those changes the result of learning or are they experience-independent developmental changes? To test the role of auditory experience in driving intrinsic changes, patch-clamp experiments were performed comparing HVC neurons in juvenile birds with varying amounts of tutor exposure. The intrinsic physiology of HVC neurons changed as a function of tutor exposure. Counterintuitively, tutor deprivation resulted in juvenile HVC neurons showing an adult-like phenotype not present in tutor-exposed juveniles. Biophysical models were developed to predict which ion channels were modulated by experience. The models indicate that tutor exposure transiently suppressed the Ih and T-type Ca2+ currents in HVC neurons that target the basal ganglia, whereas tutor exposure increased the resting membrane potential and decreased the spike amplitude in HVC neurons that drive singing. Our findings suggest that intrinsic plasticity may be part of the mechanism for auditory learning in the HVC. More broadly, models of learning and memory should consider intrinsic plasticity as a possible mechanism by which the nervous system encodes the lasting effects of experience.