Artificial protein blocks pain response
Researchers in the Department of Anesthesiology and Critical Care Medicine at the Hopkins medical school have created an artificial protein that shows promise in reducing pain associated with inflammation, which is an important and common cause of chronic pain.
The protein, called Tat-PSD-95, is able to disrupt the interactions of two important components of the inflammatory pain pathway in nerve cells. This experiment could serve as a model for future pain therapies.
The group, led by Roger Johns, translated their understanding of a simple biochemical pathway into a possible therapy. NMDA receptors, a protein found in the membranes of neurons, trigger signaling pathways inside these cells when they are activated. NMDA signaling pathways are involved in learning and memory.
"As an anesthesiologist, I have a great deal of interest in understanding the mechanisms of pain. We treat or prevent acute pain everyday in the operating room. Chronic pain is different. There is a learning process that takes place so that once you feel pain once, there is a sensitization such that the pain is intensified the next time you get a painful stimulus or the pain actually persists in the absence of a stimulus," Johns said.
Johns and his colleagues reasoned that blocking the NMDA receptor from activating its associated intracellular signaling cascade might prevent a learned inflammatory response.
"The NMDA channel receptor is involved in memory in the hippocampus of the brain but also in the spinal cord where it plays a role in the plasticity that leads to pain memory. We studied the NMDA receptor in the spinal cord and how it links to other signaling molecules inside the cell to cause these unwanted pain memories."
They targeted postsynaptic density protein-95, or PSD-95, a protein that ensures the attachment of NMDA receptors to internal signaling molecules at neuronal synapses, the point of contact between two neurons.
By disrupting these interactions between NMDA receptors and PSD-95, the researchers hoped to see decreased inflammation as well as a reduction in pain-related behavior in mice.
The protein, called Tat-PSD-95, is able to disrupt the interactions of two important components of the inflammatory pain pathway in nerve cells. This experiment could serve as a model for future pain therapies.
The group, led by Roger Johns, translated their understanding of a simple biochemical pathway into a possible therapy. NMDA receptors, a protein found in the membranes of neurons, trigger signaling pathways inside these cells when they are activated. NMDA signaling pathways are involved in learning and memory.
"As an anesthesiologist, I have a great deal of interest in understanding the mechanisms of pain. We treat or prevent acute pain everyday in the operating room. Chronic pain is different. There is a learning process that takes place so that once you feel pain once, there is a sensitization such that the pain is intensified the next time you get a painful stimulus or the pain actually persists in the absence of a stimulus," Johns said.
Johns and his colleagues reasoned that blocking the NMDA receptor from activating its associated intracellular signaling cascade might prevent a learned inflammatory response.
"The NMDA channel receptor is involved in memory in the hippocampus of the brain but also in the spinal cord where it plays a role in the plasticity that leads to pain memory. We studied the NMDA receptor in the spinal cord and how it links to other signaling molecules inside the cell to cause these unwanted pain memories."
They targeted postsynaptic density protein-95, or PSD-95, a protein that ensures the attachment of NMDA receptors to internal signaling molecules at neuronal synapses, the point of contact between two neurons.
By disrupting these interactions between NMDA receptors and PSD-95, the researchers hoped to see decreased inflammation as well as a reduction in pain-related behavior in mice.
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Janet Warren
posted 11/14/08 @ 6:37 PM EST
May God bless the people doing this research. As one who has had chronic pain for twenty years, I live in hope of real help for my pain.
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