Habecker Lab

Research

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?