We are answering several questions related to physical remodeling of sympathetic neurons after myocardial infarction:
- What are the molecules and signaling pathways that trigger the loss of nerve fibers adjacent to the infarct?
- What are the molecules and signaling pathways that cause nerve sprouting and hyperinnervation?
- Does the aberrant distribution of innervation contribute to arrhythmias?
We are answering several questions related to chemical plasticity of sympathetic neurons:
- Why are the enzymes that make NE high in neuron cell bodies but low in the left ventricle next to the site of tissue damage?
- What are the transcription factors that mediate inflammatory cytokine effects on the enzymes and transporters important for NE production and removal?
- Why is the peptide galanin elevated in the heart after myocardial infarction?
- Does galanin affect sympathetic or parasympathetic transmission in the heart?