Sympathetic nerves are lost in the damaged myocardium (infarct) after myocardial infarction (MI), and the relative area of denervation predicts risk of sudden cardiac arrest due to arrhythmias leading to the hypothesis that sympathetic reinnervation of the infarct could reduce arrhythmias. This dissertation also describes an attempt to use genetically encoded FRET-biosensors to understand signaling pathways downstream ofTrkA altered by CSPGs. Due to a number of technological challenges, we limited our assessment to Protein Kinase A (PKA) and Protein Kinase C (PKC) sensors in primary sympathetic neurons but we did not observe any significant responses to CSPGs.