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Glial cells contribute to pain
Pain hypersensitivity can spread to unaffected body regions immediately surrounding the initial insult. Sometimes it can even spread to the opposite site of the body or to large body areas and cause widespread pain. Kronschläger et al. discovered a form of synaptic plasticity in the spinal cord that may explain the spread of pain hypersensitivity. This plasticity was induced by the activation of glial cells. The spread was mediated by gliotransmitters that diffuse widely, even reaching the cerebrospinal fluid at biologically relevant concentrations.
Science, this issue p. 1144
Abstract
Learning and memory formation involve long-term potentiation (LTP) of synaptic strength. A fundamental feature of LTP induction in the brain is the need for coincident pre- and postsynaptic activity. This restricts LTP expression to activated synapses only (homosynaptic LTP) and leads to its input specificity. In the spinal cord, we discovered a fundamentally different form of LTP that is induced by glial cell activation and mediated by diffusible, extracellular messengers, including d-serine and tumor necrosis factor (TNF), and that travel long distances via the cerebrospinal fluid, thereby affecting susceptible synapses at remote sites. The properties of this gliogenic LTP resolve unexplained findings of memory traces in nociceptive pathways and may underlie forms of widespread pain hypersensitivity.
