Unravelling the neural circuits that drive increases in sympathetic nerve activity in heart failure

This project will investigate which cardiovascular brain centres are activated in the short and long term after myocardial infarction. 


For this project we will be asking the following questions:

Which areas of the brain are activated in the short and long term after a myocardial infarction?

What are the chemical phenotypes of activated neurons?

Can this neuronal activation be prevented using the anti-inflammatory compound pentoxifylline?

Heart failure (HF) is a major global healthcare problem because of its high prevalence, morbidity, mortality and cost. Patients with heart failure are three times more likely to die within three years than patients diagnosed with cancer. While there has been some improvement in HF treatment over last 30 years, morbidity and mortality remain high. One of the major contributors to disease progression is the rise in sympathetic nerve activity. However, the brain areas responsible for this detrimental increase in sympathetic nerve activity has not been well characterised.

This project will be relatively demanding and involve using a number of different techniques including surgery, echocardiography, neuroanatomy and electrophysiology if time permits. The successful completion of the project will increase our understanding of the neural circuitry driving sympathetic nerve increases in heart failure.


Techniques involved:

small animal surgery (induction of myocardial infarction)


tissue sectioning

immunohistochemistry (DAB and fluorescence)

microscopy (light, fluorescence, confocal)

 in vivo electrophysiology (if time permits)

Further Reading:

Ruchaya et al. (2014) Experimental Physiology, 99(1) 111-122.

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