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No DREAM, No pain. Closing the spinal gate
Michael Costigan1, Clifford J Woolf
1Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Massachusetts General Hospital-East, Charlestown, MA 02129, USA.
Cell
|February 21, 2002
Summary
The transcriptional repressor DREAM normally suppresses pain-reducing dynorphin in the spinal cord. Removing DREAM reduces pain behavior by allowing dynorphin to be expressed, showing how intracellular molecules control pain signals.
Area of Science:
- Neuroscience
- Molecular Biology
- Pain Research
Background:
- Spinal cord pain transmission involves a balance of facilitatory and inhibitory neural influences.
- The somatosensory system's neural circuits are key to pain modulation.
- Intracellular molecules significantly impact pain gating mechanisms.
Purpose of the Study:
- To investigate the role of the transcriptional repressor DREAM in regulating pain.
- To determine the effect of DREAM on prodynorphin expression in spinal cord neurons.
- To elucidate the contribution of intracellular molecules to spinal pain gating.
Main Methods:
- Utilized knockout models to eliminate DREAM function in spinal cord neurons.
- Measured prodynorphin expression levels in the spinal cord.
- Assessed generalized pain behavior in experimental models.
Main Results:
- Constitutive suppression of prodynorphin expression by DREAM was observed.
- Knockout of DREAM led to increased dynorphin expression.
- Sufficient dynorphin expression resulted in a significant reduction in generalized pain behavior.
Conclusions:
- DREAM acts as a key repressor of prodynorphin, thereby influencing pain perception.
- Dynorphin, regulated by DREAM, plays a critical role in reducing pain signaling.
- Intracellular transcriptional repressors like DREAM are crucial targets for modulating spinal pain gating.
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