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Gliogenic LTP spreads widely in nociceptive pathways
M T Kronschläger1, R Drdla-Schutting1, M Gassner1
1Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090 Vienna, Austria.
Science (New York, N.Y.)
|December 10, 2016
Summary
Scientists discovered a new form of long-term potentiation (LTP) in the spinal cord, triggered by glial cells and spreading through cerebrospinal fluid. This gliogenic LTP may explain widespread pain and memory traces in pain pathways.
Area of Science:
- Neuroscience
- Cellular Biology
- Pain Research
Background:
- Long-term potentiation (LTP) is crucial for learning and memory, typically requiring simultaneous pre- and postsynaptic activity for synapse specificity.
- This homosynaptic LTP mechanism is well-established in the brain but does not fully explain certain neurological phenomena.
- Unexplained memory traces in nociceptive pathways and widespread pain hypersensitivity suggest alternative plasticity mechanisms may exist.
Purpose of the Study:
- To investigate a novel form of LTP in the spinal cord.
- To identify the inducers and mediators of this spinal cord LTP.
- To explore the potential role of this new LTP form in pain hypersensitivity and memory.
Main Methods:
- Induction of LTP via glial cell activation in the spinal cord.
- Analysis of diffusible extracellular messengers, including d-serine and tumor necrosis factor (TNF).
- Tracing the long-distance travel of mediators via cerebrospinal fluid (CSF).
Main Results:
- A distinct form of LTP, termed gliogenic LTP, was identified in the spinal cord.
- Glial cell activation was found to induce this LTP.
- Diffusible messengers like d-serine and TNF, traveling via CSF, mediate gliogenic LTP, affecting remote synapses.
Conclusions:
- Gliogenic LTP in the spinal cord operates differently from brain LTP, utilizing glial cells and long-range signaling.
- This mechanism provides a potential explanation for memory traces observed in pain pathways.
- The findings suggest gliogenic LTP may underlie widespread pain hypersensitivity.
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