ScienceDaily (Jan. 30, 2011) — A powerful new painkiller, which was developed on the basis of the research conducted at Stony Brook University and with no apparent side effects or addictive qualities, may now be only a year or two from the consumer market.
"This offers a major paradigm shift in the control of pain," declares Dr. Simon Halegoua, Professor of Neurobiology & Behavior at Stony Brook who in the 1990s, teamed up with fellow Stony Brook professors Dr. Gail Mandel and Dr. Paul Brehm to identify a novel sodium ion channel involved in the transmission of pain. They predicted that a drug aimed at blocking this channel, PN1/Nav 1.7, would control pain. PN1 (Peripheral Neuron 1), is uniquely expressed in peripheral nerves such as those involved in pain transduction.
"When a patient is given an opiate like morphine, pain signals are still transmitted from sensory nerves to the central nervous system. Morphine action throughout the brain reduces and alters pain perception, but it also impairs judgement and results in drug dependence," explains Halegoua, also director of the Center for Nervous System Disorders at Stony Brook University. "With drugs targeting the PN1/Nav1.7 sodium ion channel, the pain signals would not be transmitted, even by the sensory nerves. And since the central nervous system is taken out of the equation, there would be no side effects and no addictive qualities."
The potential for such drugs is enormous -- the reduction or elimination of pain for patients with cancer, arthritis, migraine headaches, muscle pain, pain from burns, and pain from other debilitating diseases.
He notes that drugs in both oral and topical ointment forms, based on the research he conducted in a basement laboratory at Stony Brook with Mandel, a molecular biologist, and Brehm, an electrophysiologist, are currently in Phase II clinical trials in England and Canada.
To read the rest of the article:Researchers led by Hanns Zeilhofer at the University of Zurich in Switzerland found the compound after exploring the way pain signals travel up to the brain via the spinal cord.
"Normally the spinal cord acts as a kind of filter, ensuring that not all painful signals coming from the periphery of the body reach the brain," said Zeilhofer.
Neurological gatekeepers
If these neurological gatekeepers were totally absent, even the lightest touch on the skin would make us wince with discomfort, he explained. "We would be in constant pain without them."
But in patients with chronic pain, this filter function is impaired, meaning that the spinal cord is like an open channel for pain signals, he said.
A key role in the inhibition process is played by two nervous-system chemicals, called neurotransmitters. One is gamma-aminobutyric acid, also known as GABA, and the other is glycin.
"We thought we could restore the filter function if we pharmacologically enhance the action of GABA or glycin in the spinal cord," said Zeilhofer. But as no compounds had been developed that target glycin, they focused instead on GABA.
In experiments reported in the British journal Nature, the researchers induced inflammation in the paws of mice and rats, and then gauged the force needed to make the animal withdraw its leg, creating a rough measure of pain.