Brock laboratory: Autonomic and sensory neuroscience


Research Overview

The major focus of the research group is the effects of nerve injury on tissues innervated by the autonomic nervous system.  In particular, the research groups is investigating  the effects of spinal cord injury on blood vessel function and urinary bladder function.  We demonstrated for the first time that spinal cord injury produces a marked augmentation of neurovascular transmission; a change that almost certainly contributes to unusual high blood pressure episodes (autonomic dysreflexia) in spinal cord injured people.  Currently we are  investigating of the effects of spinal cord injury on the epethelial lining (urothelium) of the urinary bladder.

The research group's work also focuses on sensory transduction in polymodal and cold-sensitive receptor nerve terminals of corneal sensory neurons. These studies use a combination of electrophysiological recordings from the sensory nerve terminals, high resolution imaging and molecular approaches to investigate the mechanisms of sensory transduction in the naked nerve endings of C- and A delta-sensory neurons.


Nicole Kerr,  Research Assistant


Dr Jason Ivanusic, Department of Anatomy and Neuroscience, The University of Melbourne
Professor John Furness, Department of Anatomy and Neuroscience, The University of Melbourne
Professor Robert Shepherd, Bionics Institute/Medical Bionic Department, The University of Melbourne
Professor Helen O'Connell, Department of Surgery, The University of Melbourne
Professor Glenn Edwards, School of Animal and Veterinary Science, Charles Sturt University


Institute for Safety, Compensation and recovery Research - Improving Bladder Health After Spinal Cord Injury. CIA James Brock
Australian Research Council Linkage Project - Development of an electrode for stimulation of a transplanted neosphincter. CIs James Brock, Glenn Edwards, Robert Shepherd. PIs Christine Hirst, Helen O'Connell

Research Publications

  1. Carr RW, Pianova S, McKemy DD, Brock JA. Action potential initiation in the peripheral terminals of cold-sensitive neurones innervating the guinea-pig cornea. Journal of Physiology 2009; 587: 1249-1264.
  2. Tripovic D, Pianova S, McLachlan EM, Brock JA. Transient supersensitivity to alpha-adrenoceptor agonists, and distinct hyper-reactivity to vasopressin and angiotensin II after denervation of rat tail artery. British Journal of Pharmacology 2010; 159:142-153.
  3. Rummery NM, Tripovic D., McLachlan EM & Brock JA.  Sympathetic vasoconstriction is potentiated in arteries caudal but not rostral to a spinal cord transection in rats  Journal of Neurotrauma 2010;  27: 2077-2089.
  4. Tripovic D, Al Abed A, Rummery NM, Johansen, NJ,  McLachlan EM, Brock JA. Nerve-evoked constriction of rat tail veins is potentiated and venous diameter is reduced after chronic spinal cord transection  Journal of Neurotrauma 2011; 28: 821-829.
  5. Tripovic D, Pianova S, McLachlan EM, Brock JA.  Slow and incomplete sympathetic reinnervation of rat tail artery restores the amplitude of nerve-evoked contractions provided a perivascular plexus is present.  American Journal of Physiology: Heart and Circulatory Physiology 2011; 300, H541-554.
  6. Al Dera H, Habgood MD, Furness JB, Brock JA.  Prominent contribution of L-type Ca2+ channels to cutaneous neurovascular transmission that is revealed after spinal cord injury augments vasoconstriction. American Journal of Physiology: Heart and Circulatory Physiology 2012; 302: H752-762.
  7. Ivanusic JJ, Wood RJ, Brock JA. Sensory and sympathetic innervation of the mouse and guinea pig corneal epithelium. Journal of Comparative Neurology 2013; 521: 877- 893.