John  Griffin, M.D.

Professor of Neurology

Telephone Number:   (410) 614-3466

Fax Number:   (410) 614-0672

Johns Hopkins Hospital

Dept. of Neurology

600 N. Wolfe St.

Baltimore, MD 21205

Room: 6-113 Meyer Bldg.

Our group studies the peripheral nervous system (PNS) from the standpoint of basic cellular events in normal nerve and nerve disease. The PNS offers an accessible and relatively simple system in which to ask questions of general applicability to neurobiology. We have focused on the mechanisms of axonal organization and maintenance and the basis for axonal degeneration in disease. Ongoing studies are examining:

• The influences on the synthesis, axonal transport, and axonal modification of neuronal cytoskeletal proteins such as the neurofilaments. Their synthesis is regulated in part by growth factors derived from target tissues. They are locally modified by phosphorylation within the axon to influence the caliber of the axon. 
• How Schwann cells influence axons. For example, one influence one neurofilament phosphorylation is the presence or absence of a myelin sheath. The nature of the Schwann cell/axon signal to produce this effect is a topic of study. The myelin-associated glycoprotein MAG is a key glial molecule in this interaction, and we are examining candidate receptors on the axon.
• Mechanisms underlying axonal degeneration and regeneration. The abrupt breakdown of injured axons is an active process, analogous in many ways to apoptotic cell death. Axons are gradually lost in a wide variety of neurological diseases including peripheral neuropathies and many neurodegenerative disorders. Axonal degeneration is now known to contribute to the late progressive phase of multiple sclerosis. As the basis for axonal degeneration is increasingly understood, means of axonal protection and promotion of regeneration are realistic targets of investigation.
• The basis for pain in nerve injury and disease. Painful nerve diseases are major clinical problems. We are studying the role of the small pain fibers—the C fiber nociceptors—in generating neuropathic pain, and the roles of growth factors such as nerve growth factor in amplifying neuropathic pain. We and our colleagues have developed techniques for assessing the nerve fibers within the skin that are useful both experimentally and in patients with nerve diseases.

The laboratory interacts closely with the clinical programs in peripheral nerve disease in the Department of Neurology, with pain physiology laboratories in the Department of Neurosurgery, and with laboratories in the department of Neuroscience.