| Absent external electrical and chemical inputs onto a given neuron, voltage-gated and non-voltage gated ion channels determine the excitability, and ultimately firing properties of a neuron. In conjunction with many other forms of plasticity, the homeostasis of these intrinsic properties helps neurons maintain stable activity regimes in the face of external input variability, and against sources of destabilizing genetic mutations. In this thesis, I report a mechanism by which Drosophila melanogaster larval motor neurons stabilize hyperactivity induced by the loss of the delayed rectifying K+ channel Shaker Cognate B (SHAB), by upregulating the Ca2+-dependent K+ channel SLOWPOKE. I also show that loss of SLOWPOKE does not trigger a reciprocal compensatory upregulation of SHAB, implying that homeostatic signaling pathways utilize only a subset of the ion channels available. Finally, I show preliminary results suggesting that SLOWPOKE upregulation due to loss of SHAB is dependent on nuclear Ca2+ signaling and dCREB, implying that the SLOWPOKE homeostatic response is transcriptionally mediated.;As a second independent component of my thesis work, I addressed the need for analysis tools. The rapid development of behavioral tracking acquisition systems has left a gap in the development of accompanying analysis software. The volume of data and complicated descriptors of behavioral features generated by acquisition systems make it increasingly difficult to use traditional spreadsheet software, necessitating customized, programmatic software development. Here, I demonstrate two automated software packages I developed for use in the dissection of locomotor behaviors, and the dissection of sleep behaviors from high-resolution tracking data. |
