How do our nerves conduct impulses?
Neuroscientist Bhat brings novel discoveries to School of Medicine
SAN ANTONIO (Nov. 8, 2012) — Manzoor Bhat, Ph.D., who this summer joined the School of Medicine at the UT Health Science Center San Antonio as professor and chairman of physiology and Zachry Foundation Distinguished Chair in Neurosciences, has made seminal discoveries that are shedding light on the process of central nervous system (CNS) impulse conduction and the autoimmune disease multiple sclerosis (MS).
Dr. Bhat, who along with his team of investigators moved to Texas from the University of North Carolina at Chapel Hill, discovered a number of proteins that are central to the speed at which nerve signals are conducted along CNS wiring. Damage that slows down these signals results in the symptoms of MS.
Nerve signals travel along slender fibers called axons, which are insulated by a sheath of material called myelin. In MS, the body thinks the myelin sheath is foreign and begins to attack it, inflicting lesions in multiple CNS areas. “An axon can be 1 meter long from head to toe,” Dr. Bhat said. “Loss of myelin results in disorganization of the inner axonal core and alteration of the conduction machinery, which ultimately leads to deceleration of nerve signals.” As the speed of nerve signals decreases, the severity of symptoms increases.
MS disturbances vary widely, depending on which part of the brain or spinal cord is affected and at what intensity. Blurred vision, loss of balance and inability to move a body part are among the symptoms, including loss of fine motor coordination.
Dr. Bhat’s group discovered proteins that play roles in particular facets of nerve signal conduction. One protein, called Caspr, works alongside its partner, Neurofascin 155, to create a seal for the conduction machinery. This is necessary for proper nerve conduction to occur. Another protein, Neurofascin 186, organizes an electrically sensitive region called a node. This is also vital. When genes for any of these proteins are purposely inactivated in mice, the result is loss of nerve conduction and severe paralysis.
“Unless we know all the players that organize the conduction machinery, we can’t fix anything,” Dr. Bhat said. “We have now created adult mutant mice that progressively lose nerve functions. The question is, can we restore nerve functions and rescue their mobility? We are now ready to do inducible-rescue experiments in which we will turn a gene back on in a paralyzed mouse and hope to restore nerve functions.”
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