DURHAM, N.C. -- Ice cream lovers and hot tea drinkers with sensitive teeth could one day have a reason to celebrate a new finding from Duke University researchers. The scientists have found a very small change in a single protein that turns a cold-sensitive receptor into one that senses heat.
Understanding sensation and pain at this level could lead to more specific pain relievers that wouldn't affect the central nervous system, likely producing less severe side effects than existing medications, said Jrg Grandl, Ph.D., an assistant professor of neurobiology in Duke's School of Medicine who led the research team.
Temperature-induced pain, also called thermal pain, occurs when the body's sensory neurons come in contact with temperatures above or below a certain threshold, such as plunging a limb into freezing water.
"We want to understand how either hot or cold temperatures can activate the sensors of hot and cold temperatures in the body," Grandl said.
Previous research has identified transient receptor potential (TRP) ion channels as being highly sensitive to either cold or hot temperatures. TRP ion channels are porous proteins that play a role in initiating electrical signals by controlling the flow of charged ions across the cell membrane.
It's still unclear how temperatures make this happen, but the Grandl team's research reveals that single-letter changes in DNA, called point mutations, are sufficient to make cold-sensitive TRP ion channels become sensitive to hot temperatures instead.
"There is strong interest in understanding temperature-sensitive molecules from a functional perspective because they are promising targets for developing analgesic compounds to treat chronic pain," said Grandl, who is also a member of the Duke Institute for Brain Sciences. "It is something we currently do not treat well. So, one promising strategy is to stop pain where it is initially sensed -- at that first mole
|Contact: Karl Bates|