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?
Is acetylcholine (ACh) produced in cardiac sympathetic nerves after myocardial infarction?
- Is sympathetic ACh production triggered by gp130 inflammatory cytokines?
What are the functional consequences of sympathetic ACh release in the ventricle?