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Pathway-specific bidirectional regulation of Ca2+/calmodulin-dependent protein kinase II at spinal nociceptive synapses after acute noxious stimulation.
Department of Experimental Medical Science, Division of Neuroscience, and Lund University Pain Research Center, Lund University, Lund, Sweden.ORCID iD: 0000-0003-3584-7829
Department of Experimental Medical Science, Division of Neuroscience, and Lund University Pain Research Center, Lund University, Lund, Sweden.
2006 (English)In: Journal of Neuroscience, ISSN 0270-6474, E-ISSN 1529-2401, Vol. 26, no 16, 4198-4205 p.Article in journal (Refereed) Published
Abstract [en]

An intensely painful stimulus may lead to hyperalgesia, the enhanced sensation of subsequent painful stimuli. This is commonly believed to involve facilitated transmission of sensory signals in the spinal cord, possibly by a long-term potentiation-like mechanism. However, plasticity of identified synapses in intact hyperalgesic animals has not been reported. Here, we show, using neuronal tracing and postembedding immunogold labeling, that after acute noxious stimulation (hindpaw capsaicin injections), immunolabeling of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and of CaMKII phosphorylated at Thr(286/287) (pCaMKII) are upregulated postsynaptically at synapses established by peptidergic primary afferent fibers in the superficial dorsal horn of intact rats. In contrast, postsynaptic pCaMKII immunoreactivity was instead downregulated at synapses of nonpeptidergic primary afferent C-fibers; this loss of pCaMKII immunolabel occurred selectively at distances greater than approximately 20 nm from the postsynaptic membrane and was accompanied by a smaller reduction in total CaMKII contents of these synapses. Both pCaMKII and CaMKII immunogold labeling were unaffected at synapses formed by presumed low-threshold mechanosensitive afferent fibers. Thus, distinct molecular modifications, likely indicative of plasticity of synaptic strength, are induced at different populations of presumed nociceptive primary afferent synapse by intense noxious stimulation, suggesting a complex modulation of parallel nociceptive pathways in inflammatory hyperalgesia. Furthermore, the activity-induced loss of certain postsynaptic pools of autophosphorylated CaMKII at previously unmanipulated synapses supports a role for the kinase in basal postsynaptic function.

Place, publisher, year, edition, pages
Society for Neuroscience , 2006. Vol. 26, no 16, 4198-4205 p.
Keyword [en]
pain; synaptic plasticity; LTP; LTD; substance P; electron microscopy
National Category
Neurosciences
Identifiers
URN: urn:nbn:se:liu:diva-133055DOI: 10.1523/JNEUROSCI.0352-06.2006ISI: 000236912100006PubMedID: 16624940Scopus ID: 2-s2.0-33646443675OAI: oai:DiVA.org:liu-133055DiVA: diva2:1054569
Available from: 2016-12-08 Created: 2016-12-08 Last updated: 2016-12-13Bibliographically approved

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