Inhibiting protein against chronic pain discovered
The nerve cells in our spinal cord have a previously unknown protective mechanism against severe pain, reports an international research team led by Anke Tappe and Rohini Kuner from Heidelberg University Hospital. The discovery opens up completely new perspectives for the treatment of chronic pain.
The scientists looked at the so-called "Homer" proteins, which were discovered in the limbic system of the cerebrum nine years ago. Emotions and the perception of pain are processed in this area of the brain. The Homer proteins act as adapter proteins that play a role in the transmission of signals from the body to the processing cell systems: they connect the receptor proteins for the messenger substance glutamate with the calcium receptors in the cell membrane via a molecular framework.
The now discovered "Homer 1a" (picture on the right, red) can prevent the formation of the Homer bridge - and thus also the development of pain memory and chronic pain.
The researchers have now been able to show for the first time that the adapter proteins are also found in the spinal cord and are involved in pain processing there. They also revealed that the small Homer protein 1a can disrupt the construction of the transport framework required for signal transmission. Homer 1a is produced in abundance by the body, especially in the case of protracted inflammation. However, if its inhibitory effect fails, pain is perceived permanently because the other Homer proteins build up a pain memory undisturbed: the pain becomes chronic.
"Until now, we only knew feedback mechanisms that increase pain," say the scientists. "With Homer 1a we identified for the first time a negative feedback mechanism in pain processing."
This is of little importance for acute pain, which is a sensible warning signal. However, chronic pain, which has largely lost its meaning and warning character, would be even less bearable without the protection of the body's own emergency brake Homer 1a.
The study shows that the higher the concentration of Homer 1a in the spinal cord, the less pain is felt. This could possibly be used therapeutically by introducing the blueprint for this protein into the affected cells in gene therapy. However, it would probably be easier to mold small parts of Homer 1a, with which he breaks down the pain bridge, and to develop them into a drug. © Heidelberg University
