FREMONT, RT*; HALE, ME; Univ. of Chicago: Building Neural Networks: The Response of the Zebrafish Startle Circuit to Ectopic Expression of Mauthner Cells

Brain evolution is thought to be constrained by the interconnectedness of neurons responsible for central nervous system function. Altering a subset of cells in a neural circuit may benefit one function but decrease performance of another. Recent studies have shown that cell duplication may provide a mechanism for brain evolution with retention of original function by creating redundant circuits. Here we examine duplication in the Mauthner cells (M-cells), key reticulospinal neurons in the startle circuit that have long been a model of simple circuit function. Specifically, we examine the organization of inhibitory cells that are key for proper startle circuit function, and address how duplicate cells are integrated into functional circuits. Misexpression of Hoxb1b in larval zebrafish has been shown to cause a duplication of Mauthner cells in rhombomere (r) 2 that are functionally redundant with normal r4 M-cells. In this study we examine changes to neural circuit organization that accompany M-cell duplication. Antibody staining and physiology indicate that neurons responsible for feedforward inhibition, PHP commissural cells normally located in r4, are duplicated with the M-cells. The spiral fiber neurons, normally located in r3 and providing feedback inhibition to r4 Mauthner cells do not appear to form contacts with r2 cells at 5 days post-fertilization, when startle behaviors of larval zebrafish are typically examined. Although, it is possible that these contacts are made later in development, we suggest that duplicate cells have limited ability to connect to appropriate synaptic partners that originate in other body segments. Supported by an HHMI undergraduate fellowship to RTF and NIH 043977 to MEH.