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The Journal of Neuroscience, July 9, 2008, 28(28):7084-7090; doi:10.1523/JNEUROSCI.5749-07.2008

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Cellular/Molecular
Translocation of GluR1-Containing AMPA Receptors to a Spinal Nociceptive Synapse during Acute Noxious Stimulation

Max Larsson^1,2 and Jonas Broman^1,3

¹Department of Experimental Medical Science, Division of Neuroscience, Pain Research Center, Lund University, SE-221 84 Lund, Sweden, ²Department of Anatomy and Centre for Molecular Biology and Neuroscience, University of Oslo, N-0317 Oslo, Norway, and ³Department of Neuroscience, Karolinska Institute, S-171 77 Stockholm, Sweden

Correspondence should be addressed to Max Larsson, Department of Anatomy and Centre for Molecular Biology and Neuroscience, University of Oslo, P.O. Box 1105 Blindern, N-0317 Oslo, Norway. Email: m.d.larsson{at}medisin.uio.no

Potentiation of spinal nociceptive transmission by synaptic delivery of AMPA receptors, via an NMDA receptor- and Ca²⁺/calmodulin-dependent protein kinase II (CaMKII)-dependent pathway, has been proposed to underlie certain forms of hyperalgesia, the enhanced pain sensitivity that may accompany inflammation or tissue injury. However, the specific synaptic populations that may be subject to such plasticity have not been identified. Using neuronal tracing and postembedding immunogold labeling, we show that a model of acute inflammatory hyperalgesia is associated with an elevated density of GluR1-containing AMPA receptors, as well as an increased synaptic ratio of GluR1 to GluR2/3 subunits, at synapses established by C-fibers that lack the neuropeptide substance P. A more subtle increase in GluR1 immunolabeling was noted at synapses formed by substance P-containing nociceptors. No changes in either GluR1 or GluR2/3 contents were observed at synapses formed by low-threshold mechanosensitive primary afferent fibers. These results contrast with our previous observations in the same pain model of increased and decreased levels of activated CaMKII at synapses formed by peptidergic and nonpeptidergic nociceptive fibers, respectively, suggesting that the observed redistribution of AMPA receptor subunits does not depend on postsynaptic CaMKII activity. The present ultrastructural evidence of topographically specific, activity-dependent insertion of GluR1-containing AMPA receptors at a central synapse suggests that potentiation of nonpeptidergic C-fiber synapses by this mechanism contributes to inflammatory pain.

Key words: central sensitization; dorsal horn; capsaicin; synaptic plasticity; LTP; electron microscopy

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Received March 8, 2007; revised May 28, 2008; accepted June 2, 2008.

Correspondence should be addressed to Max Larsson, Department of Anatomy and Centre for Molecular Biology and Neuroscience, University of Oslo, P.O. Box 1105 Blindern, N-0317 Oslo, Norway. Email: m.d.larsson{at}medisin.uio.no

Related articles in J. Neurosci.:

Change of AMPA Receptors in Spinal Nociceptive Synapses during Inflammatory Hyperalgesia

Wen Wang and Jing Huang
J. Neurosci. 2008 28: 10185-10186. [Full Text]  

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