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Full NameProfessor James Francis Xavier Jones
Organisation:University College Dublin
- physiology and non-communicable disease
- neuroscience and mental health
- bioengineering/medical devices
Postgrad Medical Specialties
- Emergency Medicine
My current funded research projects involve:
1. Rat models of neuropathic faecal incontinence and the mechanism of action of sacral neuromodulation. In collaboration with Professor Ronan O'Connell I am examining the central nervous system re-arrangements that follow pudendal nerve injury. In addition, we are stimulating lumbosacral nerve roots in humans and rats to refine an emerging therapy for certain forms of faecal incontinence (SFI)
2. Atrial volume receptors in the heart funded by British Heart Foundation.
3. 3D printing of artificial muscles (funded by Seed funding UCD).
High blood pressure is now the biggest cause of death worldwide and for most people the origin of their high blood pressure is unknown. We know that inappropriate signals from the brain to regulate blood supply may be a cause and the nerve output from the brain to organs such as the kidney becomes abnormally high. Quite why this is so is not known but it may be because of the way the in which the brain processes information from the rest of the body. Specialised nerve endings in the right side of the heart sense changes in the amount of blood coming into the heart. These nerve endings called atrial volume receptors produce nerve signals that tell the brain to stop sending the messages which cause high blood pressure. Most research concentrates on how the brain handles incoming information from these receptors and not how they are able to do this. Understanding how they do this will give important clues to what drives the increased nerve activity that leads to high blood pressure.
An important immediate regulator of plasma volume is the atrial volume receptor reflex arc. This reflex is initiated by cardiac mechanoreceptors, atrial volume receptors located at the venous atrial junction of the heart. Fibres from these receptors convey information to the nucleus tractus solitarii about the state of central venous volume. This information is then integrated centrally to effect alterations in the level of sympathetic activity. Atrial receptors are an integral part of the neural circuitry that maintains plasma cardiovascular homeostasis and may contribute to the abnormal control evident in cardiovascular disease such as hypertension and heart failure. We aim to determine which ion channels are expressed and required for action potential generation following stimulation of these receptors, using neuroanatomical labelling, immunofluorescence and an in vitro heart-vagal nerve preparation. Proteins expressed in volume receptors could provide novel drug targets for the regulation of cardiovascular homeostasis.