Development of sensorimotor integration and modulation in zebrafish

Neural control of behaviour during development is a complicated orchestration of gene expression, neuronal differentiation, axonal projection, modification of intrinsic membrane properties and connectivity of neural circuits. The studies in this thesis combined genetic, molecular, and physiological assays to investigate neuromodulation, reticulospinal contribution, and neurogenic programming of the limited behavioural repertoire of developing zebrafish. Maturation of early swimming, the change from infrequent episodes of swim bursts to a sustained “beat-and-glide” pattern, was mediated by serotonergic modulation of the spinal network. Serotonergic immunoreactivity was first detected in neurons located in the ventral spinal cord at 2 days post-fertilization (dpf). A second population of serotonergic neurons was detected in the hindbrain but these remained isolated from the spinal cord in the stages studied (2-4 dpf). Serotonergic modulation of the fictive swim pattern only occurred in 4 dpf larvae, the time when “beat-and-glide” swimming emerges, but not in younger larvae. Application of serotonin did not affect properties of activity (beat-and-glide) periods, but instead reduced the periods of inactivity between activity periods. Hindbrain reticulospinal (RS) neurons displayed four types of activity patterns during simultaneous spinal motoneuron recordings of fictive swimming activity in zebrafish larvae. RS neurons generated these activity patterns even in the absence of ascending spinal input during development. The spinal CPG network, however, failed to produce rhythmic oscillations in the presence of N-methly-d-aspartate when it developed without descending RS input, indicating that the latter are necessary for development of CPG activity. In addition to swimming, zebrafish larvae also produce startle responses in reaction to potential danger, a behaviour that is missing in hi472 mutant larvae. hi472 mutation disrupt