2003 Research Fellow

2002 Frank Z. Bagan Research Fellow

Robert Dodd, MD
Stanford University

Research Title: The Role of K_CA Channels in Chronic Cerebral Vasospasm

I'm interested in the role of calcium activated potassium channels (K_CA) in subarachnoid hemorrhage induced delayed cerebral vasospasm. The mechanism by which blood surrounding the vessels induces spasm remains unknown. There is evidence that K_CA channels modulate arterial tone by antagonizing vessel contraction, thus potentially inhibiting vasospasm. We hypothesize that abnormal contraction of the vascular smooth muscle may result from potassium channel dysfunction. Reactive oxygen species (ROS) produced from heme oxidation of blood may contribute to vasospasm, and peroxynitrite, a free radical, can directly inhibit K_CA channel unitary conductance. We plan to examine the role of K_CA channel function by using transgenic knockout mice in which the regulatory subunit (ß1) of the K_CA channel is deleted.

Click here to view  Final Research Report  (PDF 144KB)

About Robert Dodd

Robert Dodd was born and raised in Chicago, Illinois. He received his secondary education at the Massachusetts Institute of Technology, obtaining a B.S. degree in Mechanical Engineering. Upon completion, Robert matriculated to Stanford University Medical School where he obtained M.D. and Ph.D. degrees in Neurosciences. His doctoral thesis examined mechanisms of signal transduction in retinal rod photoreceptors by measuring light induced changes in the membrane currents in transgenic mice. This work helped clarify the role of two proteins,
Arrestin and Recoverin in the phototransduction casasde.

Robert is currently a fifth year Neurosurgery resident at Stanford Medical Center. He is interested in Cerebrovascular Disease, and is studying the molecular mechanisms of cerebral artery vasospasm. Specifically, he is studying calcium activated potassium channels in cerebral vascular smooth muscle, and what role they may have in chronic cerebral artery vasospasm by using transgenic knockout mice deficient in these proteins.