No biological system in the body exists in isolation, but systems are often studied separately for convenience or pedagogic purpose. The nervous and the immune systems interact extensively and continuously. In this rapidly developing field of neuro-immunology, we study mechanisms and functional implications of signaling between neurons and glia or leukocytes in peripheral and central components of the nervous system (an arbitrary division), with chronic pain as major clinical focus.

Biography

Carl Saab is an active neuroscience researcher. He graduated in 1997 from the American University of Beirut (AUB) in Lebanon with an M.S. in neuroscience. At AUB, he learned the principles of pain research, devoting his time to working closely with Dr. Nayef Saadé at the department of human morphology. He then traveled to the University of Texas Medical Branch in Galveston to pursue graduate studies in the field of pain research under the guidance of Dr. William Willis. Carl obtained his Ph.D. in 2001; his decision to join the department of neurology at Yale University as a postdoctoral fellow in 2001 allowed for his collaboration with Dr. Stephen Waxman, studying basic mechanisms of neuronal degeneration and pain. Currently Carl is Assistant Professor-Research at Rhode Island Hospital Department of Surgery and Brown University Department of Neuroscience.

Research Description

The focus of our research is chronic pain due to nerve injury, referred to as neuropathic pain. Pain is a critical national health problem, the most common reason for medical appointments with nearly 40 million visits/year and over $100 billion/year in health care direct costs and lost productivity (NIH). Hospitalized patients with intractable pain experience increased length of stay and longer recovery time with deleterious effects on the immune system.

Neuronal activity underlies sensory experiences, including pain. However, glia provide homeostatic support for neurons by regulating extracellular pH, ion, and neurotransmitter concentration, acting as 'sensors of pathology' in the nervous system. Accordingly, glia contribute in a fundamental way to neurodegenerative diseases and other neurological disorders, including neuropathic pain.

We study crosstalk between neurons and glia or leukocytes in the central and peripheral nervous systems, progression from peripheral nerve injury to central nervous system plasticity, and neuro-immune signaling leading to altered neuronal processing of sensory information. We form a large team with our collaborators using surgery, behavioral paradigms, histology, imaging and electrophysiology both in vivo and in vitro to combat neuropathic pain and other neurological disorders.

Awards

- Travel award, Baltic Summer School, Kiel, Germany August 16-30, 2003.
- Young Investigator Travel Support, American Pain Society (APS) April 19-22, 2001.
- Young Investigator Travel Support and Citation Poster award, (APS) November 2-5, 2000.
- Travel award, International Society for Magnetic Resonance in Medicine (ISMRM), May, 1999.
- Travel award, International Association for the Study of Pain (IASP) 9th World Congress on Pain, Vienna, Austria, August, 1999.
- Travel awards (2), University of Wisconsin Symposium on Health and Emotion, Madison, Wisconsin, 1998-99.
- Certificate of Achievement in Teaching, UTMB, Physiology, Allied Health School, Spring, 1998.
- Who's Who Among Students In American Universities & Colleges (# 11 187-24-0-99), 1998.

Affiliations

Visiting Lecturer, American University of Beirut, Lebanon, 2-14/3-10 2004; 1-27/2-12 2006.

Funded Research

Rhode Island Foundation, "Mechanisms of Neutrophil Recruitment to Dorsal Root Ganglia after Nerve Injury", 1/1/06.

National Institutes of Health-National Institute of Neurological Disorders and Stroke, R01 NS055251-01 (D. Lipscombe, PI), "N-type calcium channel in nociceptive neurons", 7/1/06 – 3/31/10.

Stryker Dev., "Vagal Nerve Stimulation ", 4/12/2006.

NIH, R21, "Development of neuroprotective PDZ-domain inhibitors for the treatment of MS", 10%, PI John Marshall, 7/1/08 (pending)

Teaching Experience

Lecturer (6-hrs), Brown, Neuroscience (BN205): Advanced Systems Neuroscience, Neuroscience, December 30, January 1/7/8 2005.

Courses Taught

• Advanced Systems Neuroscience (BN0205)
• Advanced Systems Neuroscience (BN205)

View My Full Publication List in pdf format

Selected Publications

• Hains B.C.*, Saab C.Y.* and Waxman S.G. Changes in electrophysiologic properties and sodium channel Nav1.3 expression in thalamic neurons after spinal cord injury. Brain 128: 2359-71, 2005 (* equal contribution)(2005)
• Saab C.Y., Craner M.J., Kataoka Y. and Waxman S.G. Abnormal Purkinje cell activity in vivo in experimental allergic encephalomyelitis. Exp Brain Res 158:1-8, 2004(2004)
• Saab C.Y., Park Y.C. and Al-Chaer E.D. Thalamic modulation of visceral nociceptive processing in adult rats with neonatal colon irritation. Brain Res 1008: 186-192, 2004(2004)
• Saab C.Y. and Waxman S.G. Potentiation of sural nerve A action potential after neurogenic inflammation. NeuroReport 15: 1773-1777, 2004(2004)
• Saab C.Y. and Willis W.D. The cerebellum: organization, functions and its role in nociception. Brain Res Rev 42-1: 85-95, 2003(2003)
• Saab C.Y., Cummins T.R. and Waxman S.G. GTPγs increases Nav1.8 current in small diameter dorsal root ganglia neurons. Exp Brain Res 152: 415-419, 2003(2003)
• Lo A.C., Saab C.Y., Black J.O. and Waxman S.G. Phenytoin protects spinal cord axons and preserves neurological function in experimental allergic encephalomyelitis. J Neurophysiol 90: 3566-3571, 2003.(2003)
• Saab C.Y., Cummins T.R., Dib-Hajj S.D. and Waxman S.G. Molecular determinant of Nav1.8 sodium channel resistance to the venom from the scorpion Leiurus quinquestriatus hebraeus. Neurosci Lett 331: 79-82, 2002(2002)
• Saab C.Y. and Willis W.D. A visceral nociceptive input to the cerebellum: Possible functional significance? J Pain 2 (2;sup1): 32, 2001(2001)
• Saab C.Y., Kawasaki M., Al-Chaer E.D. and Willis W.D. Cerebellar cortical stimulation increases spinal nociceptive responses. J Neurophysiol 85: 2359-2363, 2001(2001)
• Burton A.W., Lee D.H., Saab C.Y. and Chung J.M. Preemptive intrathecal ketamine injection produces a long-lasting decrease in neuropathic pain behaviors in a rat model. Reg Anes & Pain Med 24(3): 208-13, 1999(1999)