James A McRoberts, Ph.D.

Researcher I, David Geffen School of Medicine at UCLA; Research Physiologist; West Los Angeles VA Medical Center, CURE: Digestive Diseases Research Center
 

Contact Information

Center for Neurovisceral Sciences & Women's Health
Warren Hall, Room 14-103
900 Veteran Ave.
Los Angeles, CA 90095
Tel: (310) 267-4834 (Office)
Tel: (310) 825-4786 (Lab)
Fax: (310) 267-4835
E-mail: mcrobert@ucla.edu
Web: www.cure.med.ucla.edu, www.uclacns.org, www.uclamindbody.org


Biosketch

 

James A. McRoberts is a Research Biochemist in the Department of Medicine at UCLA and director of the Cell Biology laboratories of the Neuroenteric Disease Program. Dr. McRoberts received his Ph.D. in Biochemistry from the University of California, San Francisco in 1979 and then moved to UC San Diego for postdoctoral studies in membrane transport physiology. Dr. McRoberts has a long-standing interest in cellular physiology of the gastrointestinal tract beginning in 1982 when he produced a series of research papers defining the cellular transport mechanisms involved in epithelial chloride ion secretion. He then went on to explore the role of insulin-like growth factor in regulating epithelial permeability and in its role in mediating hyperplasia of smooth muscle cells during inflammation of the colon.

In 1998, Dr. McRoberts shifted his principle area of research to neurobiology of the gastrointestinal tract. Currently, his major focus is on the role of peripheral NMDA and other glutamate-activated ionotropic receptors in mediating nociceptive responses to mechanical distension of the GI tract. These studies are aimed at developing a better understanding the mechanisms involved in enhanced perception of visceral pain (hyperalgesia) that commonly occurs in patients with functional and inflammatory bowel disorders. In patients with functional visceral disorders, such as irritable bowel syndrome (IBS), there is no detectable structural or inflammatory changes that might explain the chronic visceral hyperalgesia to mechanical stimuli. Together with Dr. Emeran Mayer and a number of local and international collaborators, we have developed a series of observations that strongly suggests that NMDA receptors on primary afferent nerve terminals in the colon participate in mechanical sensitivity and nociception. We are using a translational approach by combining in vivo, in vitro and ex vivo techniques to address this hypothesis. Dr. McRoberts is also currently leading the Animal Models Core which has developed a rat model that closely mimics many of the main features of patients with IBS including visceral hyperalgesia and enhanced colonic motility in response to stress.

 

Selected References

Chaban VV, McRoberts JA, Ennes HS, Mayer EA. Nitric oxide synthase inhibitors enhance mechanosensitive Ca2+ influx in cultured DRG neurons. Brain Research, 903: 74-85.

McRoberts JA, Coutinho S, Marvizón JCG, Grady EF, Tognetto M, Sengupta JN, Ennes HS, Chaban VV, Amadesi S, Creminon C, Lanthorn T, Geppetti P, Bunnett NW, Mayer EA. Role of peripheral N-methyl-D-aspartate (NMDA) receptors in visceral nociception in rats. Gastroenterology, 120: 1734-1748, 2001.

Marvizon JC, McRoberts JA, Ennes HS, Johansson T, Corneliussen B, Jinton L, Mayer EA. Subunit composition of NMDA receptors in rat dorsal root ganglia. J Comp Neurol 2002;446:325-341.

Coutinho SV, Plotsky PM, Sablad M, Miller JC, Zhuo H, Bayati AI, McRoberts JA, Mayer EA. Neonatal maternal separation alters stress-induced responses to viscerosomatic nociceptive stimuli in the adult rat. Amer J Physiol Gastrointest Liver Physiol 2002;282:G307-G316.

Million M, Grigoriadis DE, Sullivan S, Crowe PD, McRoberts JA, Zhou H, Saunders PR, Maillot C, Mayer EA, Tache Y. A novel water-soluble selective CRF(1) receptor antagonist, NBI 35965, blunts stress-induced visceral hyperalgesia and colonic motor function in rats. Brain Res. 2003; 985:32-42.