Dr Rasheda A Chowdhury

Miss Chowdhury read Natural Sciences at Cambridge University with Part II in Pharmacology in 2003. She then gained an MSc in Pharmacology at University of Oxford in 2004. She is currently working as a Research Assistant and studying part time for a PhD in Cardiac Electrophysiology with Professor Nicholas Peters.

Her interests lie in the correlation between gap junction remodelling and conduction abnormalities in the heart.

The heart is an essential organ responsible for sustaining the circulatory system by acting as a pump. Cardiac myocytes have the unique property of acting as a syncytium, allowing the heart to provice repeated coordinated contractions. To act in this way cardiac myocytes must undergo cell-to-cell coupling.

Gap junctions provide cell to cell pathways for propagation of electrical activity. Gap junction channels are constructed from two hemichannels, termed connexons, containing six rod-like proteins subunits (connexins) orientated to perpendicular to the membrane. A connexon in the membrane of one myocytes docks to the connexon in a neighbouring myocyte to form a low resistance pathway via which action potential propagation can occur.

Cardiac arrhythmias are a group of conditions in which the muscle contraction of the heart is irregular, or faster or slower than normal, preventing the heart from carrying out its role of sustaining circulation. Abnormal electrical conduction through the heart can lead to arrhythmias. Due to the essential role of gap junctions in action potental propagation, gap junction abnormalities can lead to arrhythmias. 

An understanding of gap junctional structure and function during normal and abnormal cardiac pacing is essential in the control of arrhythmias. My work involves assessing changes to GJs during modulation of structure & pacing.