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Can Smart Be Painful? At least in mice, the two seem somehow linked
By Nicolle Charbonneau
TUESDAY, 30 January (HealthScout) -- Does a membership in Mensa mean you're more vulnerable to chronic pain?
New research on mice suggests that those genetically altered to have better memories have a stronger response to pain.
This could lead to new treatments for chronic pain, the researchers say, through targeting of a particular brain receptor.
The possibility of a neuronal connection between pain and memory began to intrigue Min Zhuo, associate professor of anaesthesiology at the Washington University School of Medicine in St. Louis, US. He studied the molecular basis of memory and pain modulation, using genetically altered mice created in 1999 by a group of researchers at Princeton University.
Nicknamed "Doogie," after the young genius on the now-defunct American television series Doogie Howser, MD, the mice had good memories. The scientists had altered their genetic structure to produce higher-than-normal levels of a brain protein called NR2B, boosting the function of switches found on brain cells called NMDA receptors and improving their memory.
Zhuo wanted to know how these mice would respond to sensory stimuli such as pain.
To measure pain response, his research team first compared how the smarter mice and normal mice responded to acute pain, and found no difference. They then observed how often each type of mouse licked at the site of an injury during three chunks of time in a two-hour period.
The least-painful stimulus produced no significant difference, and they found no significant difference in how the smart mice responded for the first 55 minutes after a more painful stimulus.
However, in the third chunk of time, lasting from 55 minutes to two hours after the injury, the smart mice continued to lick the injury site more than twice as often, the study says.
When touched gently on the previously stimulated area, mice that first had received a non-painful stimulus showed no signs of other pain in this area, Zhuo says. However, the smart mice -- which had received a painful stimulus first -- reacted strongly to this second touch, as if it were itself causing pain. Findings appear in the February issue of Nature Neuroscience.
But does this indicate true chronic pain? The researcher who developed this strain of smart mice isn't convinced that "Doogie" responds so differently.
"In animals, it's very difficult to assess chronic pain," says Joe Tsien, an assistant professor of molecular biology at Princeton. "I'm not sure whether a small increase in the number of lickings at the third phase really means chronic pain."
"They present no convincing data regarding the chronic pain," Tsien says. "If people are interested in using NMDA- or NR2B-based strategies for the development of future memory drugs, at an early stage based on no solid data, you don't want to conclude that you will have more pain. That's misleading."
Zhuo admits that this study may not represent findings of "chronic" pain. " 'Persistent' pain may be more appropriate," he says. "[But] this experimental approach provides a model. I would never say that this is an exact copy of what would happen in a human."
"Pain deserves more attention," says Zhuo, who adds that medicine sometimes focusses on treating the disease rather than the often-debilitating symptom of pain.
What To Do
For an explanation of compounds that block the NMDA receptor, visit the Web site for the Society for Neuroscience.
And for information on chronic pain, try the North American Chronic Pain Association of Canada.
Or, you might want to read previous HealthScout articles on pain or an earlier article on the NMDA receptor.
SOURCES: Interviews with Min Zhuo, PhD, associate professor, department of anaesthesiology, anatomy & neurobiology, Washington University School of Medicine, St Louis, Missouri; and Joe Z Tsien, PhD, assistant professor, department of molecular biology, Princeton University, Princeton, New Jersey.; February 2001 Nature Neuroscience Copyright © 2001 Rx Remedy, Inc. Last updated 1/30/2001 1:00:00 AM.
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